Good morning, ladies and gentlemen, and thank you for standing by, and welcome to Allogene Therapeutics' Foruth Quarter 2019 Conference Call. [Operator Instructions] Please be aware, that today's conference is being recorded. I would now like to turn the conference over to Christine Cassiano, Chief Communications Officer. Ms. Cassiano, please go ahead.

Thank you, operator, and good morning. Before market opened today, Allogene issued a press releases, that provides a corporate update and financial results for the fourth quarter and full-year ended December 31, 2019. The press release is available on our website at www.allogene.com. We remind listeners that today's call is being webcast on our website and will be available for replay. Joining me on the call today are Dr. David Chang, President and Chief Executive Officer; Dr. Raphael Amado, Executive Vice President of Research and Development and Chief Medical Officer and Dr. Eric Schmidt, Chief Financial Officer. During today's call we will be making certain forward-looking statements. These may include statements regarding the success and timing of our ongoing and planned clinical trials, regulatory filings, future research and development efforts and manufacturing capabilities and 2020 financial guidance among other things. These forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These and other risks are described in our periodic filings made with the Securities and Exchange Commission, including our Form 10-Q for the quarter ended September 30, 2019, as well as our upcoming Form 10-K for the year ended December 31, 2019. You are cautioned not to place undue reliance on these forward-looking statements and the company disclaims any obligation to update such statements. I'll now turn the call over to Dr. David Chang.

Good morning and thank you for taking time to join us on our call today to discuss our fourth quarter and the year ahead. I am extremely pleased with what we have accomplished in 2019. We completed the hiring of senior management, built world-class capabilities to close critical functions and initiated the build-out of our GMP cell manufacturing facility in New York, California, making steady progress towards bringing the facility online in 2021. Most importantly, we initiated two clinical programs, ALLO-501 in relapsed/refractory non-Hodgkin lymphoma and ALLO-715 in relapsed/refractory multiple myeloma. Our research team is also working towards advancing additional programs and next generation cell engineering technologies which we plan to introduce into clinical trials in the coming years. It is still early in 2020, but we are continuing the momentum we created last year and working at an accelerated pace. This year, we anticipate reporting initial data for two key clinical programs, ALLO-501 in the second quarter of this year and ALLO-715 in the fourth quarter. We also look-forward to expanding our clinical portfolio as we progress on our next IND candidate ALLO-316, which targets CD70. All 200 plus employees in Allogene remain singularly focused on one goal making, ALLO CAR T therapy and their lifesaving potential a reality for patients. The team at Allogene intends to strengthen our leadership position in ALLO CAR T therapy and we recently laid out, our three part strategy to achieve this goal. Number one; establish a platform that will be foundational to the success of ALLO CAR T therapy. Number two; validate the platform through rapid clinical development of multiple product candidates, and number three; transform the future of ALLO CAR T by advancing next generation technologies to enhance the potency and selectivity of our cells. Let me walk you through our…

Thank you, David and good morning to all of you on the call today. I'd like to start with a quick update on our lead program, ALLO-501 for Relapsed/Refractory Non-Hodgkin Lymphoma. As David noted earlier, our Phase 1 trial for ALLO-501 is ongoing and we're looking forward to sharing the initial data from these ALPHA Trial, a medical meeting in the second quarter. Well the focus of any Phase 1 dose escalation trial is appropriately on safety, we're also using this trial as an opportunity to optimize our lymphodepletion strategy. There are two things to consider. First, unlike the autologous Phase 1 trial that have the benefit of extensive academic and drug development research to lymphodepletion, the regimen [indiscernible] starting from a much earlier point and little precedence regarding the optimal cell dose and lymphodepletion regimens. The second consideration is how we can better harness one of the most differentiating tools in our platform, ALLO-647, our anti-CD52 antibody to produce the best possible outcomes. We have recently completed enrollment on the three cell dose escalation cohorts in the three plus three trial and have to move to enrolling additional patients that allows us to better understand the impact of varying ALLO-647 doses or schedule. Our translational oncology team is collecting the data necessary to evaluate several potentially important parameters. These include the depth and duration of lymphodepletion patterns [indiscernible] including NKD and T-Cell depletion recovery and AlloCAR T expansion and persistence. We believe on this historical scientific approach to understanding these biomarkers and their correlation with anti-tumor activity is essential to create the best possible outcome for patients. We are leveraging strong momentum in the execution of this trial and we intend to fully explore and elucidate the optimal treatment regimen prior to advancing ALLO-501A mentioning David’s remarks into a…

Thank you, Rafael and the morning. In addition to the brief financial overview, I will provide on the call today you can read additional detail on our fourth quarter and year-end financial results in our press release issued earlier today and in our 10-K, which will be filed with the SEC. We continue to be in a strong financial position with cash, cash equivalents and investments totaling $588.9 million as of December 31, 2019. In the third quarter, our research and development expenses were $49.4 million, which includes $6.4 million of non-cash stock-based compensation expense. For the full year 2019 research and development expense were $144.5 million, which includes $10 million in expenses associated with the signing of our Notch collaboration. The total research and development expense for the year includes $19.4 million of non-cash stock based compensation expense. General and administrative expenses were $15.2 million for the fourth quarter of 2019, which included $7.5 million of non-cash stock based compensation expense. For the full year 2019, general and administrative expenses were $57.5 million, which includes $26.6 million of non-cash stock based compensation expense. Our net loss for the fourth quarter of 2019 was $61 million or $0.58 per share, including non-cash stock based compensation expense of $13.9 million. For the full year 2019, our net loss was $184.6 million or $1.83 per share, including non-cash stock based compensation expense of $46.1 million. Turning now to financial guidance for 2020. We will continue to invest heavily in our clinical programs. By the end of this year our goal is to complete enrollment in the Phase 1 ALLO-501 Trial, progress our Phase 1 ALLO-715 Trial and initiate Phase 1 trials for ALLO-501A and the ALLO-715 combination study with nirogacestat. As noted in David's earlier comments, we also look to advance the build-out of our New York manufacturing facility. As a result, we expect our full year 2020 net losses to be between $260 million and $280 million, this includes an estimated non-cash stock-based compensation expense of $70 million to $75 million and exclude any impact from potential business development activities. With that, we will now open the call for your questions.

[Operator Instructions] Our first question comes from Marc Frahm with Cowen and Company.

Hi. Thanks for taking my questions. Maybe things to this update we're going to get in the second quarter from the ALPHA Trial. You recognizing that ultimately you do need to switch over to the 501A program. But will this data set be can mature enough that there warrant for 501A you would be able to make a decision to move forward into Phase 2 and kind of have this next steps laid out? Or is it still going to be kind of work-in progress that you need more maturity on some of these different pre-conditioning regimens and the different cohorts?

Marc, this is David. I'll take your question. I mean, the question that you're asking is a very important one. And certainly there are many different aspects that goes into answering the question. In terms of, couple of things that, how you should be thinking about is internally lymphodepletion is something that we see as a generalizable concept and that is one of the reason that in the ALPHA study we’re spending a considerable amount of effort to optimize the lymphodepletion. And as we know we have been bearing the ALLO-647 both those and those in schedule to do that, and we'll certainly have a lot of data by the time that we present findings in the second quarter. And with respect to the question of making the transition from ALLO-501 and ALLO-501A one has to realize that primary antigen receptor portion of the cost remains identical. The only thing that has changed is taking out the rituximab off-switch, which in 501 was expressed as a separate protein. So we consider this as a relatively minor change and we believe that the learnings from the 501 study will be directly translatable as we move forward with ALLO-501A and that is the reason that we believe that this can be done as an abbreviated Phase 1 study as we have said in our prior statement.

Okay. When you say abbreviated Phase 1, I mean, can you get us some clarification as to what exactly is, I mean, does that mean – I mean do you have to start from as low of a dose as you did in the ALPHA Trial, but you can go up in single patients. Do you go one dose down? Can you just do the exact regimen that you've selected from ALPHA and just reconfirm PK? Like what, what does abbreviate mean?

I think one thing that I have learned over the years that I've been involved in the CAR T trial is that, anything that we do in preclinical setting we like to confirm in the clinical studies. So when we talk about abbreviated approach exactly to that point, I mean, those escalation will be somewhat simplified and the real intent is to confirm whatever we saw in 501 can be reproduced in the 501A study. So with that certainly there'll be a more color to it as we present the data and which I think has to – you have to wait for that.

Okay. Thank you.

Our next question comes from Salveen Richter with Goldman Sachs.

Thanks, good morning. So with regard to the NHL study 501, where we're going to see data in the first half here or second quarter. Are you primarily thinking of AACR and ASCO as the presentation settings for these datasets and then for this dataset? And then secondly, as you look to taking other programs into the clinics, so the multiple myeloma program that program with SpringWorks among others, how you think about – thinking about leveraging further steps in optimization be at the pre-conditioning regimen where you could play with timing of dosing as well as duration of dosing and other aspects and any kind of non-preconditioning efforts here?

Okay. Salveen, I'm going to take the first part of the question and I will ask Raphael to answer the second question regarding how we are leveraging the learning from the ALPHA study in our other programs. The question around exactly when the data presented, and we do get that question. We are very close to the second quarter and at this point, I think it will be fair to say that the target for our presentation is either ASCO or EHA meeting.

Salveen, this is Rafael and I'm going to address your BCMA question. So there's no question that the learning from 501 can use on the BCMA program. Any customer that changes in lymphodepletion that are introducing 501 and mimicked in the 715 program. You may recall that there are other changes in lymphodepletion that were introduced at the beginning of the outset in that study, which are designed to ascertain the value of cyclophosphamide and fludarabine to rituximab [indiscernible] and ING 647 by itself. But we will be testing higher doses of ING 647 in that study as well and obviously things such as, some of kinetic PK/PD interactions, sale recovery, expansion and other parameters. We expect that the learnings from 501 will translate into 715 and therefore I think it will help us accelerate decision making as we see in the data.

Thank you.

Our next question comes from Biren Amin with Jefferies.

Yes. Hi, guys. Thanks for taking my questions. Maybe if I could start with 501, 501A. How do your yields change with 501A versus 501 and given your transduction efficiency is likely going to increase since you're not requiring the switch?

Biren, I mean you are going straight into it, a very technical question. Yes, when we change the – when you make the changes to construct viral titer and other things do change. And that's where we have a very strong process development team as well manufacturing team and all of these issues have been all worked out and I can more or less tell you that the yield that we are getting from the manufacturing is really exceeding our expectations. So I don't really see this being a major issue.

Okay. And then I guess when you present the 501 data in second quarter, I just want to ask whether there's a risk where you're going to see the cells undetectable. So when you’re seeing 2019 competitors presented early data dash where they using assay, where the cells were undetectable. So what's the risk of seeing a similar issue arise in 501?

Well, I mean, you are going into the data portion of our presentation, which we are not quite ready to talk about it. But let me just tell you in terms of cellular kinetics and vector CAR-T member, this is a topic that we have at least, I personally have been working for number of years and we took some of the necessary steps to make sure that we can get reliable biomarker data in our studies. So let me just stop there without revealing too much about exactly what we will be present. But the vector CAR-T member is one of the important components of translational research.

Okay. And then maybe if I could ask a question on BCMA. So for the GSI program when do you – I guess, when do you expect to start the Phase 1, will it be after the Q4 data from 715? And I guess, how are you planning on dosing the GSI with the CAR and I guess, David and ASH a few months ago, Fred Hodge also presented the GSI data and we saw really good responses, and also observe neurotoxic thinking about six to 10 patients. So do you anticipate that the safety profile would change with the use of GSI?

Great question. I'm going to ask answer that question. I mean, Rafael has been looking into this particular area very intensely and I feel we are pretty well quick there to embark on the baseline study. Rafael?

Yes. Thanks, David. So we plan to start this study in the second half of the year. We have a great collaboration with SpringWorks. We're pretty excited about our initial interactions with them. We think the molecule is really good, PK/PD profile. It doesn't penetrate the blood brain barrier and so these leashes of neurotoxicity. I have not really being observed this treated over 100 patients. So the profile safety wise, it's pretty well understood which is very useful when you're doing a combination trial. And as you know, they've got a registration path, which obviously the helps with regards to potential co-development. So by the time we do this combination, we probably will know a lot about both lymphodepletion and dosing and we think it would be the right time to start applying the combination to try to understand whether increasing DCMA expression actually result in superiority of our product. But so far the pre-clinical data is pretty strong and we look forward to testing this combination, which hopefully will translate into better outcomes for patients.

Okay, great. Thank you.

Our next question comes from Cory Kasimov for JP Morgan.

Hey, guys. This is Matthew on for Cory. Thanks for taking my questions. So for my first question, just wondering if you can discuss what you expect to have in hand in terms of ALLO-647 based on lymphodepletion dose levels at the time of the abbreviated 501A trial initiation. Basically I'm wondering whether you expect the lymphodepletion data to be mature enough to resolve in a more narrow range of dose levels for the abbreviated 501A study.

So, Matt, this is David. Let me take that question. I mean, we have been saying that we will be elaborating the learnings from the 501 in other programs including 501A and also definitely in the 715 programs. I mean lymphodepletion, because it's really dealing with the host lymphocyte counts before the cell are given, this is quite in our view a generalizable findings. So any learnings will be a fine stat. And to your question, as we have said in the prepared remarks, we have completed dose escalation of ALLO-501 and we are actively recruiting patients into the ultimate lymphodepletion regimen cohorts. So our current projection is that we will definitely have some inflammation and that will be leveraged in how we move forward with ALLO-501 study.

Great, thanks. And then I guess for the ALPHA Trial, what should we keep in mind when comparing the initial data set to Phase 1 data sets from the CD-19 autologous space?

Can you repeat the question? Sorry.

Just wondering for the initial ALPHA data set, what should we keep in mind when comparing this to other initial Phase 1 data sets from the CD-19 autologous CAR T space?

We’re just being little bit cautious about not talking too much about what will be presented at – when we present the 501 data. I mean, the question that you're asking is a very important one. Certainly we are trying to get the Allogene cell therapy in terms of the safety and outcome to the point that is similar, if not better than what has been reported with autologous. But you also have to realize that in a Phase 1 setting, we'll be dealing with a relatively small number of patients as well as the fact that we are bearing the lymphodepletion. So there is some different sets of inflammation. So just wait till we present the data.

Great. Thanks for taking my question.

Our next question comes from Tyler Van Buren with Piper Sandler.

Hey guys. Good morning, congrats on the progress. With respect to the ALPHA data update next quarter. Is it possible to just confirm the rough number of patients we should expect and approximately what the split between DLBCL in follicular lymphoma is? And with respect to 647, I think you mentioned you're enrolling patients in the final lymphodepletion regimen. So can you give us a sense of where 647 is in terms of the 39 to 90 big range?

So we're going too much into the details of what is to be presented. So I'm going to gain and try to limit what I say. But let me just try to get some color to your question. I mean in the prepared statement, we said that we completed the dose escalation that alone should give a patient number of nine patients minimum and certainly we are going to deal on those nine patients into dose escalations. So hopefully that gives some color about what you may see and let me also emphasize that we get asked a lot about what's the duration data that you may present, but that is going to be very dependent on when the patient gets enrolled. And there are a lot of sort of dynamic nature of how the data is evolving. But when the presentation happens, we will be presenting all the available data to the time of the data cut.

Okay. That's helpful. And then for TurboCAR, can you say anything more about it with respect to what cytokine you guys may be using or maybe how it compares to some of the other approaches using the relatively well known cytokines and why you guys chose to start with myeloma and if you plan to go into non-Hodgkin's

Yes. For competitive reasons, we're not going to talk about which cytokine but over the years we have seen many different ways to enhance and provide extra so called a Signal 3, that is driven by the cytokines to the engineered T Cells and what we have seen – what I'm seeing in the TurboCAR so far is, far better than anything else that I've seen before. So we are quite excited about this TurboCAR.

That's very exciting. Thank you.

Our next question comes from Mark Breidenbach with Oppenheimer.

Hey, good morning guys and thanks for taking the questions. David, I'm just wondering, is it realistic to expect that the lymphodepletion, depth and duration requirements will likely be universal across different indications, ALL, NHL, multiple myeloma or do you think it's more probable that we'd see sort of different lymphodepletion requirements depending on the disease?

Great question. I wish I knew the answer, I mean, although there are years of doing clinical trials, I am always surprised about the patients-to-patients or indication-by-indication differences. And that's exactly what we have to do in the Phase 1 study. So the way that used to be thinking about it, as we understand the lymphodepletion and as we, optimize the six ALLO-647, we will have a very good framework to use that information and simplify the lymphodepletion exploration in other indications. So that's how we are really leveraging their learnings from ALLO-501 in other programs. And I think that approach will be very effective in simplifying the lymphodepletion exploration and other indications.

Okay. And just a quick follow-up with regard to the ALPHA trial, I'm wondering if you're seeing a lot of screening failures due to recent rituximab exposure, and if so, would you expect enrollment in ALPHA2 to proceed at a faster rate than what you've been able to achieve in ALPHA?

Yes. Mark, this is Raphael, I'll answer the question. I think that is a very perceptive observation, but based on customer exposure, but in spite of that, our accrual has been very brisk. And we've been very fortunate to work with great investigators that have been very committed and we're at pooling actually as planned and we are exactly where we want to be with that study. Now with ALLO-501A clearly, it'll be an easier study to accrue for the reasons that you mentioned. And we anticipate that it would go faster, but investigators are able to find patients for ALLO-501 and I think it's fantastic because it's allowing us to actually elucidate all these parameters that hopefully will allow us to move with ALLO-501A quicker. So yes, I mean, you're right on your observation, but it's actually not really limiting our ability to involve in ALLO-501.

Okay. Terrific. Thanks for taking the questions.

Our next question comes from John Newman with Canaccord.

Hi guys. Good morning. Thanks for taking my question. Just had a general question, David, I know you don't want to get into too much of the details about the ALLO-501 study, but is there a chance that we've might see redosing data, when we get to look at the data in the second quarter?

A great question, we don't think it's one of the changes that we introduced into the protocol and certainly you'll see some data exactly how many patients, I'm not going to say, but you will definitely see some redosing data.

Okay, great. And then just one follow-up question, this is a little bit broader. I'm sure you remember very well back, when Kite and Novartis both had their CD19 CAR T product development in the autologous setting and there was a big debate about whether longer persistence with Novartis product with the 4-1BB CAR was going to result in better efficacy versus the co-stim that Kite was using, which was CD28 and ultimately turned out that the efficacy was almost the same. I know that we're dealing with a very different product here because this is allogeneic, but can you maybe talk a little bit about how we should be thinking about persistence and detection of the cells? Is there a certain threshold that we should be thinking about? Because I know that this is different, we have to worry about host versus graft here, but just curious how you're thinking about that?

Yes. John, the question that you are asking, that is a very complicated question to answer. I'm going to sort of answer it in somewhat different way, which is really coming from the existing experience in non-Hodgkin's lymphoma. In non-Hodgkin's lymphoma, if you have a response at month three, the likelihood that response will be maintained in longer follow-up is very high, which means that whatever the initial killing of the tumor cells that really has a great impact on the durability of the response. And that's more or less, how we are thinking about the self-persistence in this setting. And if you look at some of the oncologists CAR T data, especially with CD28 close to mostly domain containing constructs, you are talking about cell expansion and persistence, probably two to three months, sometimes a little bit longer. And if we look our own UCART19 data, that level of self persistence is something that was able to be achieved in the UCART19 study. And secondly, when we present the data, we'll detail more findings on self-resistance that we see in the ALLO-501 study.

Great. Thank you.

Our next question comes from Reni Benjamin with JMP Securities.

Hi, good morning. Thanks for taking the questions and congrats on the progress. I guess this is just a broader picture question regarding your IPSE programs and how you're seeing the allogeneic space evolve. Is this something that evolves where there's space for both, healthy donor cells and IPSE’s? Do you think that, IPSE ultimately take over, how do you see this kind of shaping out moving forward?

Well, this is Raphael, I'll give it a try, but I mean, what you are asking is still unanswered. I think, obviously the IPSE field is extremely exciting, for one, it allows us or we will allow the field to have a homogeneous product that is a well characterized and inexhaustible in theory which would transform the field. I think characteristics of the T-Cells that enlarge after IPSE differentiation that's still is being worked out. I mean, will they be similar in terms of function, persistence, et cetera, both finding T-cell, come to re-engineered and still maintain the T cell differentiation capacity, will they have the same molecules, cytokines, receptors and ligands to penetrate in [indiscernible] tumor. I think all of these things, will need to be evaluated, but we're starting to see what happens in the end case space differentiation for IPFC and we see that is promising and we're pretty excited about it. And as you know, we're working pretty hard with a Notch, which that – that collaboration is also really good start. And so in terms of how we will compared to autologous healthy donors, I think we will have to see how the future evolves. At the moment, our focus in terms of the clinical trials is using allogenic donors and we are – I think leading in recruiting and ascertaining what are the best parameters for dosing, meaningfully bleeding, issues such as the ones that have been persistent, et cetera. And we plan to bring that forward to the clinic, but it will be interesting process, and working in parallel, we expect that this technology will evolve and maybe become the future, we make like this with normal donor gene therapy as well. So I think it's a matter of sort of watching this space and it's great at least, I feel that it's fantastic that there's so many opportunities in that, the technologies are advancing to make it easier, more available to patients, which would be the case in the IPSE setting.

And just as a followup, regarding donor cells and healthy donors, I know there's a lot of work going into the lymphodepletion regimens and things along those lines – is there a still a lot of work being done in terms of the ideal donor cells and types of donors that you want? Or do you feel that's largely pretty much anchored down and everything else is you're focusing on later stage parameters to change?

Reni, let me take that question. I mean, based on the sort of successes that we are having with the manufacturing, I think we feel that, donor selection became a little bit of a less of an issue. But that is an interesting topic that we are continuing to investigate and certainly as we do more manufacturing runs, we'll have a more data point to really understand, whether there is such individuals as the super donor. But ultimately, all these learnings will be applied to how we improve continuously improve the manufacturing process, I mean, we cannot build a program based on super donors out there, that knowledge will translate into our manufacturing improvement, that's how we see it.

Got it. And just one final one for me, just going back to the redosing question, can you just talk us through, what are the – I guess, redosing protocols that you're evaluating?

So I'll take that question. So the amendment that we announced at the last call, that's a lot for redosing. In addition to dosing patients that have autologous cars in the past, we would have seen probably few patients, we are enrolling some patients that are being redosed. These are patients that have benefited or eventually develop stable disease, there are some parameters in the protocols that allow for redosing and of course the patient has to convert into [indiscernible] and we have to rule out that antibodies against the donor, but if they meet the conditions, they're eligible for redosing which is fairly simple in the allogenic setting. If they are very close to the lymphodepletion, it could be given using the lymphodepletion which is longer than previous time where the cells have recovered, then they need to be conditioned again. So we will see some of those patients, it would be I think, very informative to see how patients behave off-therapeutic on those and also likewise, how do they behave after having progressed some prior CAR therapy, which are to have the change that we have made in the amendments. We look-forward to seeing what those – what happens with those patients, but our main objective remains to understand the optimal lymphodepletion and to utilize to the maximum benefit, the flexibility of antibody, which we think it gives us a lot of flexibilities. They are STEM cells that allows for recovery of granular side, some platelets [indiscernible] and remain, maintain something lymphodepletion to allow for engraftment. So that is really I think our focus now is what is the optimal length of the depletion regimen.

Great. Thank you. And congrats on the progress.

Our next question comes from [indiscernible] with William Blair.

Hi David, Sammy on for Raj. Thanks for taking my questions and congrats on the progress. So a couple of quick ones for me, I was curious, I know it's still early, but are you guys thinking that the TurboCAR ALLO-605 program will eventually replace ALLO-715 or are you kind of thinking those two programs will advance in parallel? And then in regards to the redosing, are you redosing at the same dose or are you giving patients a higher dose upon the redosing? And then I have a quick housekeeping follow-up.

Yes. Sammy, this is David Chang and I'll take the question around ALLO-605 and ALLO-715, great question. But at this point, it's too early in terms of how we can answer it? Because we will really have to examine different approaches and how different approaches leads to different patient outcome and ultimately, based on that, we will make a decision on whether we go with one or more than one, multiple-myeloma indication provides a lot of different opportunities and I certainly believe that this is a field that can accommodate not just the first generation but the next generation in a simultaneous way. So that's one of the reason that we are really advancing up our approach towards the BCMA and multiple-myeloma.

Great.

Thank you. This concludes the question and answer session, I’d like to turn the conference call back over to management for any additional comments.

Well, thank you for joining us on this call today and you're continued support of Allogene, what we know will be an exciting year for allogenic cell therapy. Operator, you may now disconnect.

Thank you. Ladies and gentlemen, thank you for participating in today's conference. This does conclude the program, you may all log-off and disconnect.