Greetings, and welcome to the Incyte Second Quarter 2016 Financial Results Conference Call. At this time all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. It is now my pleasure to introduce your host, Mike Booth, VP of Investor Relations for Incyte. Please go ahead, sir.

Thank you, Kevin. Good morning, and welcome to Incyte's second quarter 2016 earnings conference call and webcast. The slides used today are available for download on the Investor section of incyte.com. Speaking on today's call will be Hervé Hoppenot, our CEO, who will begin with a quick strategic overview; Barry Flannelly, who leads our U.S. organization, will provide some detail on Jakafi sales during Q2, as well as reviewing the recent clinical data presented at ASCO and DHA; Steven Stein, Incyte's Chief Medical Officer, will give an update on our clinical portfolio, as well as our upcoming news flow for 2016; and Dave Gryska, our CFO, will summarize our second quarter financial results, as well as the accounting treatment of the recent ARIAD transaction in Europe. We'll then open up the call for Q&A, for which we'll be joined by Reid Huber, our Chief Scientific Officer. We'd like to remind you that some of the statements made during the call today are forward-looking statements, including statements regarding our expectations for 2016 guidance, the commercialization of our products, and our development plans for the compounds in our pipeline. These forward-looking statements are subject to a number of risks and uncertainties that may cause our actual results to differ materially, including those described in our 10-Q for the quarter ended March 31, 2016, and from time to time in our other SEC documents. I'd now like to pass the call to Hervé for some introductory remarks. Hervé Hoppenot - Chairman, President & Chief Executive Officer: Thank you, Mike, and good morning, everyone. So Incyte is in an excellent position as we enter the second half of the year. So Barry, Steven, and Dave will each provide greater detail on our financial and clinical progress. But first, I would like to spend a…

Thank you. We'll now be conducting a question-and-answer session. Our first question today is coming from Salveen Richter from Goldman Sachs. Please proceed with your question. Salveen Richter - Goldman Sachs & Co.: Thanks for taking my questions. I'm just wondering what your updated thoughts may be on presentations from the IDO in PD-L1 and PD-1 combinations and what it takes to make go forward decisions? I do know we will see the mark cohort at ESMO. And just any chance we could see data from the other three cohorts in Q4? Is that more of a 2017 event? And then just a second question here. With the failure of the Bristol study in first-line lung, how does that impact your thinking on IDO? And any thoughts of adding IDO to I-O/I-O combinations? Thanks. Steven H. Stein - Chief Medical Officer & Senior Vice President: Salveen, it's Steven. Thank you for your question. The ECHO program itself, as I've stated, is progressing very well. We'll enroll over 600 patients this year alone. The 2015 presentations at SITC and SMR on the Phase I ECHO-202 program, obviously we now have a lot of additional scan data. This has reinforced our confidence in the activity of epacadostat plus pembrolizumab in melanoma and our decision to initiate that Phase III program. As I also said, the whole study will be presented as a poster discussion at ESMO on Monday, October 10, the abstracts for which will go live on September 28. And I'll refer you to that to get that update. Obviously the entire Phase II program is a lot larger, consisting of ECHO-202, -203 and -204, which is 12 tumor types. We look at at least three aspects, obviously response rate and our time to event data. How long people are on in response in terms of progression free survival. And then the third component is the biomarker data, which is critical. So that will all combine to help us to make more informed decisions in terms of triggering further Phase IIIs. The first line data that you asked me to comment. And the reason I brought up the biomarker piece at the end is I think it speaks to the importance of using all three components to make decisions, response rate, time to event, and biomarker data. Obviously the BMS data set used a lower cutoff than Merck had used in their program. And that's something we will look closely going forward at our own data set to help us make informed decisions. As to when data will be available, we remain – through the end of this year and early next year, we'll look at these programs and find appropriate medical medians to present to that. And that's all I can tell you about at the moment.

Thank you. Our next question today is coming from Eric Schmidt from Cowen & Company. Please proceed with your question. Eric Schmidt - Cowen & Co. LLC: Maybe if I could just ask Salveen's question a little bit differently. I think in the past you had expected to have go/no-go decisions on epacadostat plus PD-1 inhibitors by year end. If you're kind of not able to hit that milestone – or maybe you still are. I don't know. But what would you say to the skeptics who say that the inability to make a decision is sort of an indictment of the program? And that you're not seeing much in terms of activity or a clear path forward? Steven H. Stein - Chief Medical Officer & Senior Vice President: Yeah, Eric, it's Steven again. And again thank you for your question. Again it's the three components that we need to make decisions, and I'll be repetitive. Response, the time that the end response, progression free survival, and the biomarker piece. We are gathering across the program all three pieces of information. Again enrollment has been as expected or better with more than 600 patients enrolled. And then there are two components. There's the sit down, we look at, and make decisions. And then when to present it at an appropriate medical median and to find that median. So I don't think it's – we're still extremely confident in the program and the opportunity. And it doesn't speak to any lack of confidence at all. It's just finding the appropriate venues. The data is coming in as expected. And again through the end of this year and early next year, we will be able to share that in appropriate venues. Eric Schmidt - Cowen & Co. LLC: Thanks, Steven.

Thank you. Our next question today is coming from the line of Geoff Meacham from Barclays. Please proceed with your question.

Good morning, guys. Thanks for the question. Not to beat a dead horse here on epacadostat, but when you look at data in other combo studies, is there a specific number of cycles that you're looking for to be the trigger for next steps? Or I guess scientifically what's the thought on the onset of action from what you've seen so far when you combine epacadostat with PD-1? Thanks. Steven H. Stein - Chief Medical Officer & Senior Vice President: Geoff, it's Steven again, and Reid may make additive comments on your second part of your question on the scientific aspects. I think you allude to – one thing we did learn last year around the SITC/SMR experience is to have a little more mature data sets beyond first scan information. Generalizing across a program, we generally do first scans at around 9 weeks and second scans at 18 weeks. And then there on. And it is around the time to event piece that's most critical here, because that tends to be the endpoint that you use in regulatory studies, including in our own ECHO-301 program, where we're looking at progression free survival as well as overall survival. So I personally favor having more mature data sets to make informed decisions. And then combining that, as you've seen critically now with the recent BMS experience, with the biomarker piece as well. So a long answer to your question. But the two scan at least piece of information is critical. And then beyond that in terms of hitting various benchmarks. I don't know if Reid wants to make anything additive to the scientific aspect of having longer data in the immuno-oncology setting, where you actually tend to focus beyond response on things like progression free survival and overall survival.

Yeah. Just one other additive comment, Geoff. This is Reid. I think that we know now in immunotherapy that – and we've come to expect that responses can occur later into treatment. So responses that are converted from patients with stable disease after a number of cycles is not uncommon. And so it's important to gather that duration of treatment data, so we can more accurately measure and quantify the benefit of a doublet regimen. So absolutely it's an important part of the program. And as Steven alluded to, it's captured in that second bucket of data, where you're looking at durability of response, where you can also convert and capture those patients that are exhibiting responses a little bit later into treatment.

Got you. Okay. Thanks, guys.

Thank you. Our next question today is coming from Michael Schmidt from Leerink Partners. Please proceed with your question.

Yeah. Thanks for taking my questions. I had one for Barry. In terms of Jakafi growth, could you just break down volume versus price versus inventory movement? And then I had one for Steven around epacadostat. Is it fair to assume – that in the Phase II program, is it fair to assume that it's biased towards indications where PD-1 is approved? And how important is it for you to make a Phase III go decision, depending on whether a partner is opting in to cost share the trial? Thanks. Barry P. Flannelly - Executive Vice President & General Manager US: Hi, Michael. It's Barry. Sure. So as you know we had a 14% growth quarter over quarter, Q2 over Q1. And we took a 6% price increase at the beginning of the second quarter. We don't get all of that 6% of course, because of mandatory government rebates and discounts and so forth. So that's about 5%. We know that the gross to net improved in the second quarter by 2.9% versus the first quarter of 2016. And we had a prescription demand increase by more than 6% in the second quarter versus the first quarter. And I'll turn it over to Steven for the next part of that question. Steven H. Stein - Chief Medical Officer & Senior Vice President: Yeah, Michael. It's Steven. I don't know if bias is the right word. But if you look across the ECHO program in its totality and the four different studies, we have 12 different tumor types there. You're correct in that many of them are considered the hotter tumors that already have approvals for PD-1 or PD-L1. So melanoma and non-small cell lung cancer, bladder cancer, and just recently head and neck. But we additionally study in other areas where we will explore the biology of areas where it is maybe not so hot from an immune aspect, like triple-negative breast cancer, ovarian, lymphoma, colorectal cancer, et cetera. And then we'll study all those end points that I alluded to earlier in terms of making decisions. But we're looking at both the hot and cold tumors. So I don't think it's biased. In terms of selecting partners for future collaborations and how to do them and whether opt-ins, or the importance thereof, I'm going to ask Hervé to address that. Hervé Hoppenot - Chairman, President & Chief Executive Officer: Yeah. Fundamentally, I mean we like to work together with a partner and to have the cost sharing program. So that's something that we are trying to get. But it would never stop us from moving into the next step of the program, if for some reason, the partner was not willing to go and do the cost sharing. So it's basically a good guy if we have it. And if we don't, we go ahead and we do it anyway, if we believe there is enough data to justify moving to the next step.

Great. Thanks so much.

Thank you. Our next question today is coming from Brian Abrahams from Jefferies. Please proceed with your question.

Hi, guys. Thanks for taking my question and congrats on a good quarter. Two questions. First off, I guess shifting gears to GVHD. Sounds like the pivotal program, steroid refractory patients, is kicking off. You mentioned we'll get some data for 110 [39110] later this year. Just wondering, where might 110 potentially fit in? Do you see a potential role for that in sort of a different segment? Perhaps in prophylactic or frontline patients? Any reason why a selective JAK1 might work differently versus ruxolitinib? Or is that just – should we just see that as proof of principle for ruxo? And then for Barry, I'm wondering as we're seeing continued survival data rollout for Jakafi, are you guys seeing an evolution in clinical practices in terms of earlier intervention in MF? And how much potential room for growth do you foresee in terms of moving towards earlier stage patients? Steven H. Stein - Chief Medical Officer & Senior Vice President: So, Brian, I'll start off. It's Steven, and Reid may make additive comments. So you're right. In terms of graft versus host disease, you have to be somewhat careful in separating out the different entities. There's the acute setting and then the chronic setting. And then within the acute setting there is steroid refractory first line and the prophylactic setting. And we feel that both compounds may potentially have a role there. In terms of the biology that may underlie that, I mean we're obviously developing the clinical data now and look forward to sharing the 39110 proof of concept data with you hopefully later this year. But that's leveraging the JAK1 versus 2 [JAK2] selectivity in terms of myelosuppression in certain settings. And we feel that 39110's best roles in that disease setting may be in first line, so prior to developing steroid refractoriness, and in the prophylactic setting, where the potential in terms of the lack of myelosuppression may be more helpful. These patients are just post transplants and tend to have lower blood count. So that's one area we may be able to leverage a different biology. And Reid may want to make additive comments there. So both prophylactic and first line. Whereas for rux itself, our current program is focusing on steroid refractory acute and then the chronic setting, which by definition is also steroid refractory. And I'll leave it to Reid, if he wants to make any more comments around the biology.

Yeah. So, Brian, thanks for the question. The data and the translational work around how JAK inhibition is having these productive effects in patients with graft versus host disease is still very much evolving. But to the extent that we've studied it and other academics have studied that, they appear to be mediated largely by JAK1 containing signaling networks. And so it's a very provocative scientific hypothesis, the study of JAK1 selective inhibitor in these diseases. As Steven said, ultimately the clinical data will tell us what the profile benefits may be of a JAK1 inhibitor versus a JAK1/JAK2. But there's certainly some emerging scientific basis to be interested in studying JAK1 inhibition in this disease. Barry P. Flannelly - Executive Vice President & General Manager US: So, Brian, it's Barry, just to address your survival data in MF. Yes, strangely, many of our prescribers are only now realizing the survival – or the benefit of starting Jakafi earlier in myelofibrosis patients. Now we have two Phase III trials, COMFORT-I and COMFORT-II, with 5-year follow up. And we have a more than 30% reduction in the risk of death by starting Jakafi earlier versus placebo followed by Jakafi or best available therapy followed by Jakafi. So we think we've penetrated the prevalence in the United States by about 25% to 28%. And we think we have a long way to go in myelofibrosis, particularly to benefit those patients who might start therapy earlier.

Thanks very much.

Thank you. Our next question today is coming from Alethia Young from Credit Suisse. Please proceed with your question. Alethia Young - Credit Suisse Securities (USA) LLC (Broker): Hey, guys. Thanks for taking my question and congrats on a good quarter. Just one around that new ASCO SITC conference in February. Do you think that's a potential venue where we could get some more clinical information for epacadostat? And the second one. I just wanted to talk a little bit about the duration of treatment for Jakafi? I just wanted to see if like you kind of are starting to see kind of increased duration with kind of some of the longer term data that you've been presenting? And then also on p-vera [polycythemia vera], just wanted to – wanted you to talk about the same trend there as well. Thanks. Steven H. Stein - Chief Medical Officer & Senior Vice President: Alethia, it's Steven. Re the ability to present epacadostat at various meetings, that is an interesting meeting. And our eye is on it. We in general will not speak to whether things will be at the meeting until the meeting itself releases its abstract data. So I'll just leave it at that. And pass it to Barry for your second question. Barry P. Flannelly - Executive Vice President & General Manager US: Yeah. We've talked about persistency for both MF and PV. Continues to get better year over year for both MF and PV. I think I've said before that the PV persistency is a little bit longer. Obviously we look to our Phase III clinical trials as one signal. And in fact in both response and in COMFORT-I, COMFORT-II, the patients stay on therapy for a long period of time. So we try to keep patients on therapy, because we think they'll continue to benefit. Obviously the survival benefit that we've shown in myelofibrosis and then in terms of symptom control and seize control that we've seen in response and response to, we think this persistency will only continue to get better.

Thank you. Our next question is coming from Tony Butler from Guggenheim. Please proceed with your question.

Yes. Thanks very much for taking the questions. So I would love to get your view on the GITR agonist, especially potentially in combination with, say, an anti-PD1. Given the notion that there are a number of inflammatory events that may occur with PD-1 alone, perhaps pancreatitis, stemonitis (36:20), et cetera. So the question really is, do you get – do you think you may get or obtain excess -itis, whatever -itis, simply because you're adding effectively two agonists together? Would love to understand that view. And then second, with respect to bladder cancer on the FGFR inhibitor, really around selectivity, given that there are a couple of other competitors in the market with FGFR inhibitors? And more importantly, why bladder cancer first is a first line? I recognize there are a number or a percentage of bladder cancers, which certainly have FGFR3. But the question really is why bladder cancer first? Thanks.

Yeah. Hi, Tony. This is Reid. I'll take both your questions, and Steven can chime in with additional comments at the end. I think first with respect to GITR, it's – and we're learning a little bit more about the agonist space after this last ASCO, including data presented on the OX40 agonist. But there's an outstanding I think question in the field up until these clinical data, as to what the ultimate safety profile and tolerability may be of a co-stimulatory agonist. And the data at least emerging thus far from OX40 and maybe soon to emerge around GITR is encouraging in that respect. So that's the first thing to note. And I think that's important for the field to recognize, is that these antibodies appear to be able to be delivered, at least as single agents, as safe treatments with early signs of pharmacologic or pharmacodynamic activity. As you know the ultimate utility of these antibodies, based on preclinical data, is likely in combination. And you referenced the PD-1-based combinations, which are clearly attractive combination approaches for both GITR and OX40. It's where our program is certainly designed to move to. And we think that the most relevant go/no-go decisions and true understanding of safety and efficacy is probably going to come from data emerging from those combination regimens. Whether there is an inflammatory or an -itis type toxicity is yet to be determined. But certainly the monotherapy data is encouraging. And then we're going to have to look for the actual clinical combination data to speak to that, because as you know preclinical data doesn't really read on safety. On your next question with respect to FGFR, 54828 was brought forward – designed to and was brought forward, because it's a very selective inhibitor of three FGFR…

Thank you, Reid. That's helpful.

Thank you. Our next question today is coming from Simos Simeonidis from RBC Capital Markets. Please proceed with your question.

Hi, guys. Thank you for taking the question. This has been I think kind of asked earlier in a different way. But what I wanted to get your thoughts on is, whether you're currently doing anything differently post the – surprise to many people – failure of the Bristol drug in front line lung cancer in your trials with PD-1, PD-L1 inhibitors in lung cancer? And the second question is, I know Mike Booth has communicated in the past how you guys will talk to us about which combinations you might take into next steps with epacadostat. But is it still going to be in a staggered fashion? Is it going to be all at once? And then we get the data? Is there any changes to that? Thank you. Steven H. Stein - Chief Medical Officer & Senior Vice President: Simos, hi. It's Steven answering your question. I think in terms of first-line lung cancer, and this is more a general comment. Sometimes it can be advantageous to not be out front, because you can learn from other data sets, not necessarily failures but just other data sets. And in this case I think at least in lung cancer as opposed to melanoma, the quantitative intensity of the staining may be more important than it is in other histologies. And where the cut-offs lie and how they inform your drug and its activity is going to be really, really important. So the obvious answer is, yes, we will be looking in depth at the biomarker parts of the lung cancer program and trying to understand where we differentiate on efficacy? And where we add, is it at the same cut-offs or different cut-offs? And that work's in progress at the moment. In terms of combinations, and I'll let Reid add to this. It's really, it's wide open. We will look at different levels of evidence. There's preclinical cell line evidence, then xenografts, and then clinical evidence, either from ourselves or collaborators, and where we will work in both hot and cold tumors and in combination in terms of enhanced in other compounds. The majority of the program right now is on PD-1 and PD-L1 combinations. But there are others in development, including triplets, where we look at our own small molecules in different dosing schedules to see if we can modulate the tumor marker environment by looking at paired biopsies and enhance immune responses. And then we have a vaccine program as well in combination with vaccines. And it's not step-wise. I mean we're willing to look at things as soon as the evidence is available. And we remain very confident in that opportunity. I don't know, Reid, if you want to add anything around combinations. But hopefully that answers your question.

Great.

Our next question today is coming from Cory Kasimov with JPMorgan. Please proceed with your question.

Hey. Good morning. This is Morgan on for Cory. I just wanted to ask a quick question on the data presentation at ESMO. You've referenced potentially for us to see PFS data. Are we going to see medium PFS? Or are we going to see any sort of percent PFS at certain time points? Steven H. Stein - Chief Medical Officer & Senior Vice President: Yeah. Morgan, it's Steven. Obviously, wait for the presentation is the high level answer. Again it's on poster discussion on Monday, October 10. If you look at the SITC and SMR data sets, we now have additional scan data. And we'll be able to look at progression free survival over a much longer time interval. As for the actual data, I'll refer you, one, to the abstract when it goes live on September 28, and then the actual presentation.

Okay. Great. Thanks.

Thank you. Our next question today is coming from Ying Huang from Bank of America Merrill Lynch. Please proceed with your question.

Hey. Good morning, guys. I have a question on whether you have any preclinical data or clinical data you have seen so far, that's not a float to show, there's a row for IDO (45:13) inhibition for PD-L1 negative or even the low expression of PD-L1 tumor types. And then secondly, I was wondering if you can provide any more color on the decision by your partner, Lilly, to drop a couple indications, including diabetic nephropathy, and then move on for another two indications, including atopic dermatitis and lupus. Thanks.

Yeah. Hi, Ying. I'll start off with your first question. This is Reid on the preclinical data. So IDO has been studied in a number of tumor models now. And they really range across both what we think of as hotter, more inflamed tumors, and tumors which are characterized by less of productive immune cell infiltrating more of a myelosuppressive or immune suppressive immune cell infiltrate. The reproducibility of IDO synergy with PD-1 is a very common finding. We in fact see it when tumors are IDO1 positive. We see it impact when tumors are IDO negative, where the IDO activity may be coming from the infiltrating immune cells and from the tumor draining lymph node. So I think that data set is a fairly robust one. The question is, how those models translate to patients? And there as you well know, we have to be much more cautious in either over or under interpreting the preclinical data. So the approach that Steven has outlined and we're following with the ECHO program is to not to limit histology selection and the expansion cohorts to only those which have been shown to be PD-1 responsive or only those which are characterized by cold tumors or PD-L1 negative status. We tend to look at both of those. And then use a more robust translational program on the back end to work through those details. I think that's a strength of the program going forward. So we're not biased based on any pre-clinical – pre-conceived notions, and I'll turn the next question over to Hervé. Hervé Hoppenot - Chairman, President & Chief Executive Officer: Yes. Concerning the Lilly relationship. I mean you have to remember that the way it works is that we would be asked at some point when the program is going to Phase III to either opt in or not in co-financing of the Phase III. Before that we are literally in a position where we give our opinion and our advice. But we are really not in any kind of decision position, so I cannot comment on their willingness to go for any of these indications. But as we said, I think we are dealing with a very broad list of possible indication for this mechanism. And really – and we are discussing with them about it, are certainly looking at multiple places where baricitinib could be applied. I mean the decisions to drop nephropathy recently, something that was not a huge surprise from our side.

All right. Thanks.

Thank you. Our next question today is coming from Peter Lawson from SunTrust Robinson Humphrey. Please proceed with your question.

Steven, just with the BMS failure. wondering if you could walk through the biomarker strategy you have around epacadostat, as well as GITR and if there's any points of differentiation you have in that biomarker strategy? And how you could potentially drive positive outcomes with the strategy? Steven H. Stein - Chief Medical Officer & Senior Vice President: Yeah. Peter, hi. It's Steven. I cannot speak to the specifics of each collaboration and granular details on the biomarker strategy. Just to tell you that it's broad. So it's beyond immunohistochemistry and staining and quantitative staining intensity. And we're looking other aspects, including the genetics of the space and trying to get a comprehensive understanding of where therapies work and why they don't. Obviously the cutoff per se in the first line lung of the one compound at BMS versus Merck's compound in interesting. Is it 5% or 50%, and what that difference means? And then looking at it in combination. And then the same for GITR. We have a comprehensive program, but it's too early to give you any specifics.

And just a follow-up around that. Is there a chance that you can go back and change the cutoff rate, manipulate that? Or are you kind of locked in? Steven H. Stein - Chief Medical Officer & Senior Vice President: So in terms of the exploratory part of the program now, it's hypothesis generating. So it's not a question of changing anything. We can look respectively across the board. When you trigger a prospect of Phase 3, then you have to prospectively set what you're going to be looking at. Just to be clear our melanoma's Phase 3 ECHO-301 doesn't use any selectivity in terms of PD-L1 staining. And that's not really relevant in the melanoma space at the moment. But there's no cutoff in the Phase 2 programs. It's we're doing across the board hypothesis testing.

Great. Thank you so much.

Thank you. Our next question today is coming Ren Benjamin from Raymond James. Please proceed with your question. Reni Benjamin - Raymond James & Associates, Inc.: Good morning and thanks for taking the questions and congratulations on a great quarter. I guess one question for Barry. Barry, can you give us a sense at all or any color regarding the split of MF versus PV? And you mentioned the 6% prescription increase in the quarter. Is that growth coming from one indication more than the other? And then one for Steve, just regarding the IDO studies, will you be presenting the data based on the trials as a whole or specific to these cohorts? So for example, would you present data from ECHO-2O2 and ECHO-203, the triple negative breast cancer, all at the breast cancer conference at the end of this year, but from two different trials? And I guess final question regarding bladder cancer. Can you give us any sort of detail or color? Is it muscle invasive, non-muscle invasive, or superficial? Or in combination with BCP? Barry P. Flannelly - Executive Vice President & General Manager US: Hi, Ren. In terms of a breakdown of MF and PV, we still have more sales in MF, just because the total cohort of patients that we had over time, they continue to grow. As I said before, the persistency is good. But in terms of growth quarter over quarter, it's a greater – PV is now – the total number of PV patients' growth is outpacing the total growth of MF patients. But they're both still growing quarter over quarter. And we think we can actually increase that going forward, particularly for the overall survival in MF and now additional data in PV. Reni Benjamin - Raymond James & Associates, Inc.: Got it. Barry P. Flannelly - Executive Vice President & General Manager US: Steven? Steven H. Stein - Chief Medical Officer & Senior Vice President: Ren, it's Steven for your second and third question. In terms of when and where and how to present the IDO data sets, it's really a case-by-case discussion with our partners and the investigators. To date, we've generally presented studies as a whole. So if you look at SITC last year, the ECHO-202 experience, and then what's coming up at ESMO this year. But going forward, there may be opportunities around histologies. It's just too early to speak to whether for example, you do a single histology, other histology relevant medians, like a breast median. But again it's a discussion with our partners and investigators. In terms of bladder cancer the current program is directed at metastatic bladder cancer. It's not superficial or non-muscle invasive. The unmet need in the metastatic setting at the moment. We will going forward look at potential other areas to study. But that's where the program is at the moment. Reni Benjamin - Raymond James & Associates, Inc.: Got it. Thank you.

Thank you. Our next question today is coming from Ian Somaiya from BMO. Please proceed with your question.

Thanks. And congratulations on a great quarter. I had two questions. First for Hervé. Just want to get your sense, I mean just your ability – do you think you have the ability to at this point continue to aggressively fund your growing oncology portfolio, as well as take advantage of the options that you have in terms of the baricitinib program? And just (54:01) question just related to your financial health. Do you think you can do both at the same time? And then separately for Reid. I was just hoping to get your thoughts on some of the early sort of microbiome data that's been published? And potential for combination with the different I-O's programs? Hervé Hoppenot - Chairman, President & Chief Executive Officer: Yeah, Ian. Hervé. So, yeah, on the financial heath, I mean you can see the numbers yourself. I mean what – we are in a position where the growth of the top line is giving us a lot of flexibility to invest in our own portfolio. And if Lilly would decide to go in additional indication, which I wish obviously, we would be able to also do the co-funding. To give you an idea, from last year to this year, in fact the co-funding of the Lilly program has gone down, because of the cycle in rheumatoid arthritis. So if we were to go in new indication, there would be no problem to do that. I mean the way we are thinking of resource allocation is obviously top line growth is what's giving us all of these opportunities. We spoke about ruxolitinib, but we have also now hopefully if baricitinib is approved next year, there will be a new line of top line growth from the royalties and some of the milestone from Lilly. We think about portfolio kinetics, how to move the portfolio as fast as possible in the right indication, obviously based on the scientific understanding we have. So we are not limiting our clinical program, because of resource constraints at this point. Based on what you have seen this quarter, you can see we have room to maneuver. And obviously we stay in a positive cash flow from operations. I mean that's important, because that's sort of what makes us stable from the financial standpoint for – and able to do this operation. So that's the three criteria that we are using. And up to now, it has been there something we can – we have been able to manage very positively. So the answer is yes. If there were opportunities to do co-funding with Lilly, we would probably participate, assuming the indication is reasonable.

And, Ian, this is Reid. I'll take your second question. So I think – so our view of the microbiome data are that they're very interesting. Obviously some of it has come from a close collaborator of ours, Dr. Tom Gajewski at University of Chicago. It's not an area which we have built a particular expertise around. So I think we look at the data and how it emerges in the context of our combination possibilities, much like we look at other platforms, such as vaccines or cellular therapeutics. Some of these may emerge as interesting tools. And when they emerge into the clinic, we'll always evaluate the science behind them, and how we may be able to work together in those sorts of combination strategies. But right now I think it's a little bit early to assign any real strong scientific rationale to specific combination possibilities that may be appropriate for us.

Thank you. Our next question is a follow-up from Michael Schmidt from Leerink Partners. Please proceed with your question.

Yeah. Thanks for taking my follow-up. I just had one. So you mentioned the importance of PFS information and assessing the efficacy of epacadostat in combination with JAK1 inhibitors. And just wondering, number one, looking at the upcoming data at ESMO, can you just remind us of the benchmarks of what would you expect for PD-1 alone in terms of PFS in those patients? And then secondly, PD-1 inhibitors historically have been, I believe at least, most efficacious in prolonging overall survival, as opposed to PFS. And I'm just wondering what your thoughts are here in terms of the – sort of the PFS as a measure that you're considering. Thanks. Steven H. Stein - Chief Medical Officer & Senior Vice President: Yeah. Michael, it's Steven. It's one of the three components of progression free survival or time to progression. The benchmarks, if you look at pembro alone and generalizing, because you have to be very specific about exactly what population you look in. And then are you enriching for particularly biomarker expression. But in general if you look at their label in melanoma, you're looking at about 6 months for pembro alone. If you look at nivo plus ipi in the same setting, you're looking at about 11.5 months for that combination. And then obviously with efficacy, you always weigh in toxicity in terms of getting to your risk elements sort of equation in terms of using therapies. But those are the numbers we bear in mind in terms of getting there. And again I'll refer you to the actual presentation. From a tolerability point of view, to date, our data is very encouraging versus other doublets. You're right. In terms of overall survival, that is ultimately what is most important to patients and often to regulators. You just can't wait in terms of decision making early on to wait for OS, and they're not – they tend not to be randomized studies. So you use surrogates like response and progression free, which we feel is most important in terms of decision making.

Okay. Great. Thanks for the follow-up.

Thank you. We've reached the end of our question-and-answer session. I'd like to turn the floor back over to Hervé for any further or closing comments. Hervé Hoppenot - Chairman, President & Chief Executive Officer: Okay. Thanks, all of you, for time today and for your question. And just conclude saying that we look forward to providing you with further data, where our Q3 call in early in November. And for now, thank you and goodbye.

Thank you. That does conclude today's teleconference. You may disconnect your line at this time, and have a wonderful day. We thank you for your participation today.