Welcome to the Alnylam Pharmaceuticals Conference Call to Discuss First Quarter 2016 Financial Results. There will be a question-and-answer session to follow. Please be advised that this call is being taped at the company's request. I would now like to turn the call over to the company. Christine Regan Lindenboom - Vice President, Investor Relations & Corporate Communications: Good afternoon. I'm Christine Lindenboom, Vice President of Investor Relations and Corporate Communications at Alnylam. With me today here are John Maraganore, Chief Executive Officer; Barry Greene, President and Chief Operating Officer; Akshay Vaishnaw, is actually under the weather today so joining us will be Pushkal Garg, Senior Vice President of Clinical Development and Mike Mason, Vice President and Treasurer. In addition, DA Gros, Senior VP, Chief Business Officer, is in the room and available for Q&A. For those of you participating via conference call, the slides will be made available via webcast and also be accessed by going to the Investors page of our website, www.alnylam.com. During today's call, as outlined on slide two, John will provide some introductory remarks and provide general context, Pushkal will summarize recent clinical progress, Mike will review our financials and Barry will provide a brief summary of goals for 2016 and beyond before opening the call for your questions. I would like to remind you that this call will contain Alnylam's future expectations, plans and prospects, which constitute forward-looking statements for the purposes of Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in our most recent Annual Report on file with the SEC. In addition, any forward-looking statements represent our views only as the date of this recording and…

Thanks, John, good afternoon, everybody. We indeed continue to make great progress with our pipeline of RNAi therapeutics. Let me begin with our programs in our genetic medicine STAr and start with our therapeutics for the treatment of TTR-mediated amyloidosis. As you know, we have multiple product candidates in this area. First, Patisiran. As John mentioned, we completed enrollment in the APOLLO study early in the first quarter and affirmed our previous guidance that we expect to report data in 2017. If APOLLO is positive, we expect to submit an NDA and MAA for Patisiran in late in 2017. As reminder and as shown on slide seven, the APOLLO Phase III trial is a randomized, double-blind, placebo-controlled global study designed to evaluate the efficacy and safety of Patisiran in patients with hereditary ATTR polyneuropathy. The primary endpoint of this study is the difference in the change in a modified Neuropathy Impairment Score or mNIS+7 from baseline to 18 months between Patisiran and placebo. The study was significantly over-enrolled with a total of 225 patients with Stage 1 or 2 disease compared to the original anticipated enrollment of 200. Turning to the new results presented from our Phase II open-label extension study at AAN, we were very pleased to show continued evidence for potential halting of neuropathy progression. Specifically, as highlighted on slide eight, there was mean decrease in the mNIS+7 Neuropathy Impairment Score of 0.8 points which compares favorably to an estimated mean increase in mNIS+7 of 22 to 26 points over 18 months based upon analyses of historical data sets in untreated patients with similar baseline characteristics. Similar results were observed in patients with or without concurrent tetramer stabilizer use. In addition, Patisiran administration was associated with a statistically significant approximately 77% median improvement in nerve fiber density based…

Thank you. Our first question comes from Alethia Young of Credit Suisse. Your line is open. Alethia Young - Credit Suisse Securities (USA) LLC (Broker): Hey. Hey, guys thanks for taking my question. Congrats on the... John M. Maraganore - Chief Executive Officer & Director: Hi, Alethia. Alethia Young - Credit Suisse Securities (USA) LLC (Broker): Hey. Two, since you only said two. I guess, I'm thinking about like Eculizumab and sparing versus the poor response, is that how you're going to pursue going forward in other indications in complement-mediated diseases? And the second question is like when you think about like 1210 and comparing there, like how do you think about, well do you think that your strategy would change depending on the different outcomes we could see with 1210? Thanks. John M. Maraganore - Chief Executive Officer & Director: Thanks, Alethia. Let me make some comments then Pushkal if you want to jump in as well. As it relates to the other indications, we believe that monotherapy may very well be the best path forward in these other indications. We haven't yet – obviously, we'll evaluate monotherapy and the other indications as well but there may be other settings where using it in combination with eculizumab or anti-C5 antibodies, generally speaking, would be warranted as well. But certainly, our thinking is that monotherapy would be explored in those other settings in general. And as it relates to 1210, look 1210 is still yet to be read out in terms of specific data. So we'll have to see how that looks. Clearly, the approach is that we're proposing here we think will be valuable whether it's 1210 or eculizumab alone. So it doesn't really influence too much based on what happens with 1210. Pushkal, do you want to add anything to that?

Yeah, maybe just two quick points. I think one is that PNH cells in PNH patients there is this vulnerability because of defects in CD59, so they may be particularly vulnerable. And so there may be somewhat different thresholds with other complement-mediated diseases. So I think the opportunity to pursue both monotherapy and or combination approaches as John outlined are viable there and we're going to evaluate those going forward. So, I think – and we do know certainly that there is an unmet need for patients who are not fully adequately controlled in a number of these diseases that we can potentially address of ALN-CC5. So that's what we're going to be looking to pursue. John M. Maraganore - Chief Executive Officer & Director: And I'd just add our investigators are extremely excited about the data that we'll be presenting in June in terms of the potential for both poor responders and also for sparing. And so when you see those data, you will have a better sense of why we think there is a very interesting opportunity here. Alethia Young - Credit Suisse Securities (USA) LLC (Broker): Okay, great. Thanks. John M. Maraganore - Chief Executive Officer & Director: Thank you.

And our next question comes from Terence Flynn of Goldman Sachs. Your line is open. Cameron Bradshaw - Goldman Sachs & Co.: Hi, this is Cameron filling in for Terence. Thank you for taking our question. John M. Maraganore - Chief Executive Officer & Director: Hey, Cameron, how are you? Cameron Bradshaw - Goldman Sachs & Co.: I'm well. Thank you. John M. Maraganore - Chief Executive Officer & Director: Good. Cameron Bradshaw - Goldman Sachs & Co.: Maybe first off, can you share any more data on the C5 program that led to your decision, particularly anything on knockdown or LEH changes? And then second – oh, go ahead. John M. Maraganore - Chief Executive Officer & Director: Yeah, Cameron, we have an oral presentation at EHA, which is under data embargo. So we really can't share anything beyond the top line conclusions that we've shared today. So you just have to wait till June 11 when those data are presented. Cameron Bradshaw - Goldman Sachs & Co.: Okay. And then for the C5 program, more broadly, do you have any thought of exploring additional doses or schedules? John M. Maraganore - Chief Executive Officer & Director: Sure. Pushkal, you can comment. I think we feel pretty good about the dose and dose schedules that we've got as it relates to the mechanism of our drug which is to essentially knock down liver derived C5 all the way to the floor. And so, when you have that type of a biomarker and you're getting a very complete effect through our mechanism of action, it's very easy to get to being comfortable around the right dose and right dose regimen. And we don't think, there is anything about dose and dose regimen that changes our conclusion about how we would go forward. Pushkal, do you want to add anything to that?

Yeah. I would just say we've studied and you'll see both from the Part A and B in healthy volunteers and Part C, we study a pretty broad range of doses. So I think that's very informative test as we pursue the upcoming Phase II study and some of the indications next year that we'll be pursuing and we will able to share more at EHA. Cameron Bradshaw - Goldman Sachs & Co.: Okay. Thanks for taking the question. John M. Maraganore - Chief Executive Officer & Director: All right. Thanks, Cameron.

And our next question comes from Ritu Baral of Cowen. Your line is open. Ritu Baral - Cowen & Co. LLC: Hi, guys. Thanks for taking the question. First question is on ENDEAVOUR, can you comment a little bit about the how the conduct of that study is going and dropout and compliance as you're seeing it right now probably on a blinded basis? John M. Maraganore - Chief Executive Officer & Director: Sure. We can certainly give you very broad comments on that Ritu. Obviously, as we announced today, the enrollment is going far better than we had expected. I think it's fair to say. We plan on being fully enrolled by the end of the year. We're well over 50% into the study enrollment at this point and all sides are enrolling pretty positively. Total number of sites now, Pushkal, are...

Roughly 60 or so. John M. Maraganore - Chief Executive Officer & Director: ...roughly 60 worldwide. And so it's going very well. Obviously, we've been benefited here by the continued and protracted clinical hold that Ionis are in because it's removed any competition for enrollment in the space. And while that's obviously not necessarily the best thing for patients per se from a competitive standpoint, it's obviously very good for us and for the enrollment in the study. I don't think we can really comment on discontinuation rates right now but I think we can say in general that we're pleased with the profile that we are seeing from a blinded study. There's nothing that has us concerned and that, to some extent, is reflected in the rate of enrollment that we have as well in the study. So, so far so good, Ritu. Ritu Baral - Cowen & Co. LLC: Got it. Next question is on the C5 program. John M. Maraganore - Chief Executive Officer & Director: Yeah. Ritu Baral - Cowen & Co. LLC: As you look at the Phase II that you mentioned and also potential pivotal studies for eculizumab sparing, what do you think the pivotal endpoint would be, or what do you think the endpoint is going to be for your Phase II? And what do you think is an acceptable pivotal endpoint along those lines, along those for C5 development? John M. Maraganore - Chief Executive Officer & Director: Right. Let me have Pushkal address those questions.

Hi, Ritu. So, yeah, I think it's a very interesting question. I think the nice thing about PNH is that there are clearly measurable biomarkers, the most prominent of which is LDH that can be measured in serum. And it's been associated with – it's not controlled, poor prognostic outcomes for patients with this disease. And we know based on data in the literature as well as what we're hearing from investigators if there are fair number of patients who actually don't have their LDH fully controlled and then an ongoing risk for thromboembolic events and an ongoing hemolysis. And so we think that, that is something subject to discussion with health authorities that could potentially be a registrable endpoint in PNH but there may be also opportunities to show symptom improvements. There are patients who have residual symptoms and, of course, being treated with eculizumab where combination approaches, sparing approaches may be able to – with ALN-CC5, may be able to alleviate patient symptomatology as well. So, we're going to be exploring those sorts of avenues as we build that package up and generate the Phase II data and then take that to health authorities. Ritu Baral - Cowen & Co. LLC: Got it. Thanks for taking the questions. John M. Maraganore - Chief Executive Officer & Director: Thanks, Ritu.

And our next question comes from Alan Carr of Needham & Company. Your line is open. Alan Carr - Needham & Co. LLC: Hi. Thanks for taking my questions. John M. Maraganore - Chief Executive Officer & Director: Hi, Alan. Alan Carr - Needham & Co. LLC: Hi, a couple of them. One of them, I wonder if you could elaborate a bit on AS1, what you're looking for from the Phase I data. You mentioned that Phase III might be coming up pretty soon. So if you could talk about that program a little bit more. And then, I also noticed in your press release you didn't have it in your prepared remarks but it looks like with another candidate going after HAE, I wonder if you could comment on that, too. What sort of profile you're thinking might be able to put together? John M. Maraganore - Chief Executive Officer & Director: Let me make a couple comments – let me address this last one and then, Pushkal, you can get porphyria. So with ALN-F12 which is a program that we just put into development, it's targeting Factor XII. And the goal there is to explore for hereditary angioedema, also potentially as thromboprophylaxis. There's a very interesting data set around Factor XII and its involvement obviously in thrombosis. And there's an approach there that might be worth exploring as well. We're going to look at both as opportunities. But for HAE specifically, Alan, the profile that we think we can achieve with ALN-F12 is a potential subcu quarterly drug for the prevention of attacks in patients with HAE that we think that would be a very competitive profile versus the existing drugs that are out there but also the Dyax Shire drug that's in development. So at a very high level, that's where we're going with that program but it's still preclinical. We'll obviously update you more when we get that into the clinical stages. So let me turn to Pushkal then on porphyria.

Sure. Thanks, John. So Alan on the AS1 program for porphyria, recall that the acute hepatic porphyrias really are due to defects in the heme biosynthesis pathway like in AIP specifically the defect in the enzyme PBGD. But what happens in all of these is that you get a buildup of these toxic metabolites most prominently, ALA and PBG. And that buildup of those metabolites, that's bought to, relate to the various neurovisceral symptoms that these patient get: pain, attacks, et cetera that it can be treated sometimes with hematin, et cetera although not terribly effectively in many patients. And so what we're doing with AS1 is we're looking at blocking an upstream enzyme in the pathway to prevent the buildup of this toxic intermediates, ALA and PBG. So when we think about what we're going to look for in the Phase I study, in addition to safety and tolerability, of course, we're going to be looking to see in these patients who we call asymptomatic hyper excreters in Parts A and B of the Phase I/II study and then in AIP patients with recurrent attacks in Part C of the study that we get good knockdown of ALN-AS1. But most importantly we'd like to see that we can bring those ALA and PBG levels which are elevated back close to normal. I think that's going to be the strongest indicator for us in terms of something that we're actually has a potential to be meaningful for these patients in avoiding the attacks or preventing the attacks. In Part C, we will be enrolling patients who have recurrent attacks. That's a small cohort of patients but ideally we'll be able to see even some impact in terms of attack frequency or severity in that but that is a small cohort of patients. So really what we're going to be looking at is being able to bring those levels of those toxic intermediate down closer to normal for these patients. And what we guided, Alan, is that we expect to have data in the recurrent attack patients by the end of the year. Alan Carr - Needham & Co. LLC: Your thoughts on what an endpoint might be for registration, or is it too early for that? John M. Maraganore - Chief Executive Officer & Director: Pushkal?

Well, we haven't had those discussions. So everything is subject to that discussion with the health authorities but I think we are looking at endpoints and considering endpoints that relate to – really what's most troubling to these patients which is frequent recurrent attacks and trying to prevent those from happening in patients on ALN-AS1. Those attacks often require intensive treatment, visits to urgent care facilities, hospitalizations, et cetera. And so we'll be looking at some sort of an attack-related endpoint. Alan Carr - Needham & Co. LLC: Frequency or severity, something along those lines?

Yeah, I think probably some combination of those. Alan Carr - Needham & Co. LLC: Okay. Thanks very much.

And our next question comes from Mike King of JMP Securities. Your line is open.

Hey, guys. Good afternoon. Thanks for taking the questions. Just want to start with a comment that I think Barry looks awesome with a hard hat? Barry E. Greene - President & Chief Operating Officer: Thanks, Mike.

If you're selling framed copies of that, please I'll take one but (42:30)... Barry E. Greene - President & Chief Operating Officer: We'll send you a frame signed one in the next few days.

Signed, yes. Definitely. I hate to belabor the C5 program, but I'm just anticipating the inbound questions I'm going to get about it. And I just wonder if you guys feel that you have the appropriate construct. I know that you have all the pharmacodynamic markers that you want that's typical of all of your assets. I'm just wondering if there's something unique about the biology of complement that has – going the route you're going as opposed to a monotherapy in PNH. John M. Maraganore - Chief Executive Officer & Director: I think – this is a really active drug. When you look at our Part A and B data that we presented at ASH, we're getting 99% plus knockdown of C5. It's really hard to squeeze out much more out of a biological system like a human being than that level. And so, obviously I won't refer to data in PNH which is under embargo, but there is no reason to believe that a PNH patient would be different than a volunteer in terms of that. So, there may well be factors that are related to extra hepatic supply of complement factor C5 that's in play or it could be other factors. But I think we'll have to wait till the data comes out at EHA for the clarity on that. What we can say now is that we have clinical activity. We think that the most competitive profile is as a drug to be used for sparing of eculizumab or for eculizumab poor responders. And we have data that convince us that that's a really attractive path forward as well as our KOLs. And so you'll see those data in a few weeks. EHA is not that far away. And then that will add some clarity to all that. But we do feel that the path forward at least in PNH is in that way. For other complement diseases for reasons that partly that Pushkal mentioned, it's unclear that you need to have another antibody present. It could very well be that monotherapy is fully sufficient.

Okay, thanks for the detailed answer there, John. And then just switching quickly to the TTR programs. We checked the ISA website, and it said that abstract acceptance cutoff date was April 28. So I'm just wondering is the expectation that if you get accepted for both, well, one or the other Patisiran or Revusiran that they would be accepted as late breakers. Thank you. John M. Maraganore - Chief Executive Officer & Director: I mean that's news to us on the April 28. I'm looking at Pushkal, he was equally surprised by that.

Yeah. John M. Maraganore - Chief Executive Officer & Director: But we haven't received notification yet, but that's the meeting that we're pretty active in. So I'd be surprised if we don't have both of those presentations there. I'd be shocked, but obviously we'll have to wait for the organizers to notify us formally, if that's the case. April 28 was last week. Meetings in Uppsala, mail goes slowly.

Yeah, I'm well aware of the timelines of academic organizations. They're not quite the same as ours. All right. Thanks, guys. John M. Maraganore - Chief Executive Officer & Director: Great, thank you.

And our next question comes from Michael Schmidt of Leerink Partners. Your line is open.

Hey. Thanks for taking my question. John M. Maraganore - Chief Executive Officer & Director: Hi, Michael.

Hey, how is it going? John M. Maraganore - Chief Executive Officer & Director: Good.

Just one more on C5. John M. Maraganore - Chief Executive Officer & Director: Sure.

Just to understand next step, so the Phase II trial in early 2017, so that is in both poor responders as well as well controlled PNH patients, is that correct? John M. Maraganore - Chief Executive Officer & Director: So, the goal is in 2016 by this year's end is to start that trial. And Pushkal, do you want to give some color on the current thinking?

Yeah, so Michael, the current thinking as John said is to start a Phase II study at the end of this year. That we really would be looking at ALN-CC5 in PNH patients who have somewhat – who are not fully controlled on eculizumab and looking at combination approaches both with full dose and in a sparing type of regimen to really explore that combination approach in PNH. So these will be patients who are not fully controlled with eculizumab. We understand from both literature and as well as talking to our investigators and why their investigators are excited about this is there is a substantial proportion of patients who do have artfully controlled with eculizumab where this combination approach may make sense and/or sparing approach.

Yes, that was my next question, I guess. What percentage of patients is considered poor responders? And I guess what gives you confidence that you can I guess add – that the drug works in those patients?

So I think our understanding is that it's approximately 20% to 30% of patients who actually may not have adequate control on eculizumab alone. And in terms of what gives us confidence, I think what I'd have to say is that, some of the data that we're looking that we've gotten from Part C that we'll be presenting at June 11 that unfortunately we can't speak about more about now, I think is what gives us the appreciation that this may be the best development path and an appropriate development path based on the data that we've already seen.

All right. Thanks. And then I wanted to circle back to the TTR program as well. And so with the ENDEAVOUR trial enrollment going well, I was wondering – I know you're running this genetics screener study or feeder study. John M. Maraganore - Chief Executive Officer & Director: Yes, DISCOVERY.

Right, exactly. So I was wondering what are you seeing now that you probably screened a significant amount of patients in terms of how the market looks. Does it meet the expectations in terms of the mutation frequencies that you're seeing? The patient numbers does that all add up to expectations? John M. Maraganore - Chief Executive Officer & Director: It's a great question. Pushkal, do you want to comment?

Yeah, DISCOVERY, I think what I would say is that if you recall the DISCOVERY study was really looking at patients who had sort of some characteristic signs in terms of echocardiographic or EKG changes as well as symptoms that may their – a suspicion of ATTR amyloidosis a potential for them. And I think what really was highlighted how quickly that's definitely enrolled over 1,000 patients. And I think that was really a testament that a number of patients who potentially meet have these sort of difficult to diagnose congestive heart failure types of profiles that may have cardiomyopathy. So I think that if I would say anything – others may want to chime in, it highlights actually that there's probably a pent-up demand for new therapeutics disease. And the unmet need is actually larger than we may have thought. Barry? Barry E. Greene - President & Chief Operating Officer: Yeah, I agree with that and, Michael, what I'd say is that what we're seeing for Revusiran and its cardiomyopathy is not uncharacteristic of what we've seen in other orphan diseases where diagnosis are suggested and a potential therapeutic opportunity is presented, the patient numbers seem to grow. And as you've heard there was some skepticism of how many patients were out there and even in light of another Phase III running with Pfizer, we're quickly enrolling the study. And that should be a proof point about how well we're finding these patients.

Okay, great. Thanks a lot. Barry E. Greene - President & Chief Operating Officer: Thank you.

And our next question from the Ted Tenthoff of Piper Jaffray. Your line is open. Ted A. Tenthoff - Piper Jaffray & Co. (Broker): Great. Thank you very much and thanks for the call. John M. Maraganore - Chief Executive Officer & Director: Hi, Ted. Ted A. Tenthoff - Piper Jaffray & Co. (Broker): Hey, how are you, John? John M. Maraganore - Chief Executive Officer & Director: Good. Ted A. Tenthoff - Piper Jaffray & Co. (Broker): Thanks for the thorough update. So with all the other questions focused on pipeline and all the C5 questions, I kind of want to go a different direction and ask you about the manufacturing facility. How long it's going to take to build this out and how should we be thinking about scale once you get there? John M. Maraganore - Chief Executive Officer & Director: Yeah, great question. Barry, you want to handle it? Barry E. Greene - President & Chief Operating Officer: Yeah, Ted, so we'll be operational in 2018. We're talking about state-of-the art 200,000 square foot facility on 12 acres just south of here in Norton. And the reference that Mike made earlier is we had our groundbreaking facility last week which was met with tremendous reception in Norton in Massachusetts. We'll continue to work with third-party clinical manufactures and commercial manufacturers. As you're well aware, our pipeline is growing tremendously. And particularly with some of the cardio-metabolic and hepatic infectious programs, the capacity that were need exceeds the capacity that exists today. So by having our own manufacturing facility that we could also then expand on, we meet the needs of our growing pipeline for the next five or six years to come. And clearly, if we continue to be successful there may be other manufacturing moves we make down the road but this will help us for the next five or six years for sure. Ted A. Tenthoff - Piper Jaffray & Co. (Broker): Cool. And Barry just to pick up on that point, how does this also sort of affect future potential partnering opportunities? Is this something where you guys would continue to be the manufacturer of a product? That seems to me like it could strengthen negotiating positions? Barry E. Greene - President & Chief Operating Officer: Yeah, it's a good point, Ted. In particular as we look at the larger population diseases, our ability to with effective cost of goods supply significant amount of product to this large populations will be critical to the kind of margins that any partner might be needing particularly outside the U.S. and Western European markets. So by having our own facility, we'll be able to scale appropriately. Ted A. Tenthoff - Piper Jaffray & Co. (Broker): Cool, awesome. Thanks for the update. Barry E. Greene - President & Chief Operating Officer: Thanks, Ted.

And our next question comes from Christopher James of FBR & Company. Your line is open. Christopher S. James - FBR Capital Markets & Co.: Hi, guys. Thanks for taking the question and congrats on the progress. Just two quick ones and I hate to belabor the CC5 opportunity, but quickly how do you define a poor responder? And then secondly, I'm sorry... John M. Maraganore - Chief Executive Officer & Director: Yeah, that's a great question, but you go ahead you put your second question first. Christopher S. James - FBR Capital Markets & Co.: And then, yeah, second question is just as good. How do you think about the potential combinability with eculizumab? John M. Maraganore - Chief Executive Officer & Director: Oh, good, that's a good one too. Christopher S. James - FBR Capital Markets & Co.: Told you. John M. Maraganore - Chief Executive Officer & Director: So Pushkal, do you want to handle both?

Yeah, let me start and then – so thanks, Christopher. I think in terms of ecu (54:00) poor responders, I think the way we think about that is if I'm in a couple of dimensions, certainly there are patients who, for example, are having breakthrough hemolysis symptoms within the dosing interval of an every 14-day dosing interval for eculizumab or patients who are not adequately controlled the need to have dose escalation and even in some of those instances are not fully controlled from either a symptomatology perspective or, as I was speaking earlier, there's epidemiologic data in these patients to suggest that having an LDH lactate dehydrogenase level that's more than normal, more than 1.5 times the upper limit of normal is associated with ongoing risk for thromboembolic event. And so when we think about patients who are poor responders, we think about those patients with either persistently elevated LDH and or persistent symptomatology on doses of eculizumab. So that's the first part of your question. And I apologize, what was the second question? John M. Maraganore - Chief Executive Officer & Director: The second excellent question was on combinations...

Chris, your question is how readily achievable with the combine (55:13). Christopher S. James - FBR Capital Markets & Co.: Combinable, yeah.

Yeah, and look, I think we've already in Part C. As you may recall, the study design, we actually had a period of time where we were actually giving both drugs in combination. If you are going at it from an clinical perspective, to make sure I'm understanding your question, certainly the most important thing is around safety and tolerability. These are given – one is IV, one is subcutaneously. There is no issue there. And so in terms of the consequence of a C5 knockdown or complement inhibition – those are the same; we manage these patients in terms of potential for risk for infection, et cetera, so we're not concerned in sort of in the general principle way combining these two therapies and we think that there can be additive pharmacologic effect that could be a real benefit to these patients. And I think that's some of the data that we want to speak to and it's prompting our thinking around with the development path here. Christopher S. James - FBR Capital Markets & Co.: Great. Thanks, guys. John M. Maraganore - Chief Executive Officer & Director: Great. Thanks, C.J.

And out next question comes from Anupam Rama of JPMorgan. Your line is open.

Hey, guys. This is Eric in for Anupam. Thanks for taking the question. Just a couple TTR related ones from us today. First with ENDEAVOUR, can you remind us what the allowance is for concomitant stabilizer use? And what proportion of patients you might expect to be also on stabilizers with Revusiran, and what in a way you're expecting in terms of the incremental impact? And then also I've a follow up. John M. Maraganore - Chief Executive Officer & Director: So that's a simple one. So in the protocol, patients cannot be on concomitant use of TTR stabilizers, either tafamidis or diflunisal. So it's a pure study, placebo controlled, no stabilizers in both arms.

Got it, thanks. And just a question related to the post liver transplant study in FAP patients? Just wonder if you can briefly talk about the rationale and the opportunity with that trial, and whether this might serve as a label broadening opportunity getting Revusiran into FAP? Thanks. John M. Maraganore - Chief Executive Officer & Director: Sure. Let me provide some context and then give it to Pushkal on the label broadening. But the reason we're doing that study, small study, is as we begin to advance Patisiran and Revusiran and in fact, TTRsc02 going forward, we're interested in the entirety of the TTR disease segments. And includes cardiomyopathy patients. It includes polyneuropathy patients. It includes the wild type patients that we'll certainly be exploring with TTRsc02 in the future. But there are patients also that have had a liver transplant that are progressing on their liver transplant because of the production of the wild type TTR protein. And we had quite a bit of interest from investigators for us to do something about those patients and obviously our desire is to help those patients. And so that's why we're doing the study to provide evidence that the drug can be safely administered to the population and that you know hopefully we can provide some evidence that we're stabilizing disease progression that occurs in those patients. Tragically, because these patients have no resort after having received a liver transplant, as they progress, they have nothing they can do but succumb to the disease. So that's where we're pursuing it. Pushkal, you want to comment a little bit on the regulatory label extension side of it?

Yeah, absolutely. So I think we're doing this study – it's in approximately 12 patients with Revusiran in patients who are post liver transplant. And certainly our thinking is that as we a) those data will be inherently important as they are to sort of understand both safety and tolerability and the impact of TTR lowering in these patients and whether we can have a favorable impact in terms of their disease course, but would certainly be our intent to take those data when they mature to health authorities in the context of our regulatory negotiations and pursue, labeling of the data are encouraging and show that there may be benefit to these patients. So absolutely, that would be our intent. As John mentioned, we'd really like to develop a series of therapies that will address the full range of disease manifestations of ATTR amyloidosis. And we think that this is an important aspect of that.

Okay. Great, thanks. John M. Maraganore - Chief Executive Officer & Director: Sure. Thank you.

I would now like to turn the conference to Mr. John Maraganore for any closing remarks. John M. Maraganore - Chief Executive Officer & Director: Thanks, everyone for joining us this afternoon. You 're going to hear – have a lot more data coming up this year. We already have some data in May and June, in July, which I think will be quite exciting and then stay tuned for more info on our RNAi Roundtable. Until then, have a great rest of the day. And we'll talk soon. Thanks, bye, bye.

Ladies and gentlemen, thank you for participating in today's conference. This concludes the program. You may all disconnect. Everyone have a great day.