Welcome everyone to the 40th annual JP Morgan Healthcare Conference. My name is Tessa Romero. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by Taylor Hanley from the team. Our next presenting company is Atara Biotherapeutics, and presenting on behalf of the company, we have CEO Pascal Touchon. Before I turn it over to Pascal, I just wanted to remind all the listeners to please use the ask a question button in the portal to ask your question, and I'm happy to ask it on your behalf. With that, I'd like to hand it over to Pascal. Thank you, Tessa, for the introduction, and thank you to JP Morgan team for inviting Atara to present. Happy New Year to all of you. I'm very pleased to be here today to tell you more about our industry-leading allogeneic T-cell product pipeline and upcoming catalyst. During the course of my presentation, as you can see on slide two, I will be making forward-looking statement, and I refer you to our current SEC filings. Now, on slide three, I would like to highlight that Atara is an industry-leading allogeneic T-cell company with a differentiated and scalable platform based on Epstein-Barr virus T-cells or EBV T-cells from healthy donors. Our platform is supported by extensive clinical experience as we have treated already more than 400 patients with our allogeneic T-cell therapy and have generated promising clinical efficacy and safety data in different diseases. We are, we believe, the most advanced allogeneic T-cell therapy in development with tab-cel, a first-in-kind late-stage oncology program, for which we submitted our MAA to the EMA in November of last year and were granted accelerated assessment. We also have a potentially transformative multiple sclerosis treatment called ATA188 that recently received Fast Track designation and is in double-blind randomized placebo-controlled trial. Furthermore, we have a portfolio of differentiated, potentially best-in-class allogeneic CAR-T programs, and we expect our first two allogeneic CAR-T INDs to be filed in Q4 of this year. I'd like now to move to slide six and upcoming key catalysts, as we believe that 2022 is going to be a very exciting year for Atara and the progress we are making with innovative therapy for patients. Starting with tab-cel BLA submission in Q2 of this year that we're planning and anticipated approval of tab-cel in EU in Q4 of this year. We're also eagerly anticipating the interim analysis of our MS program, ATA188, in Q2 of this year. We believe that ATA188 could be a truly transformational product for patients with multiple sclerosis and has the potential to be a multi-billion-dollar revenue opportunity if successful. We're also advancing our allogeneic CAR-T portfolio and expect to submit INDs in both our mesothelin and CD19 targeted programs in Q4 of this year. I will discuss these programs in more detail momentarily. Let's start on slide eight with tab-cel, our allogeneic T-cell product candidate that has received FDA breakthrough and EMA prime designations. We are making good progress on the regulatory front with tab-cel for patients with an ultra-rare cancer called EBV positive post-transplant lymphoproliferative disorder, or PTLD. Starting on the right side of this slide, we submitted the tab-cel MAA for patients with previously treated EBV positive PTLD with EMA in November of last year and anticipate a decision in Q4 of this year under accelerated assessment. We are working actively with our commercial partner, Pierre Fabre, to prepare for the launch of tab-cel in Europe at the end of next year. This year, sorry. With FDA, we continue to make progress, most recently through constructive engagement with CBER in Q4 of 2021. We now have a scheduled type B CMC meeting to occur in Q1 of this year and plan then to have a pre-BLA meeting and to file the BLA in Q2, with anticipated U.S. launch in the first half of 2023. On slide nine, you can see that at ASH Congress last month, we had the first presentation of positive data from the pivotal phase III ALLELE study for tab-cel. These data demonstrated a 50% objective response rate by independent oncology radiographic assessment and 89% overall survival or OS at one year in responders versus 32% in non-responders, as well as durability of response and favorable safety profile. These data have been presented to both the FDA and EMA and are supporting our MAA submission with accelerated assessment in Europe. To put such pivotal clinical data in perspective, let me highlight new data also presented at ASH in patients with EBV-positive PTLD for whom rituximab or rituximab plus chemo has failed. Where median survival is very poor with only 0.7 months, so just a few weeks for post-HCT patients and 4.1 months for post-SOT patients. This clearly means that the response rate, duration of response, and overall survival data from our pivotal study demonstrate the potential for tabelecleucel to be transformative for patients with an urgent unmet need. On slide ten, we had another overall presentation at ASH, where we showed longer-term data from our phase II and expanded access protocol studies for tab-cel, showing a median OS of approximately 55 months and similar two-year survival benefit of over 86% in responders, regardless of whether they achieve a complete response or CR or a partial response or PR. No new safety signals with more than 180 patients treated to date, including no observed related graft versus host disease or GVHD. The ALLELE pivotal study results, reinforced by the long-term follow-up of our phase II and EAP, were very well perceived by physicians during the congress, as they are eager to get a therapeutic solution for these patients in urgent medical need. They were enthusiastic about the potential for durable responses with favorable safety in patients receiving tab-cel. Now moving on to slide 12 and ATA188 or potentially transformative treatment of multiple sclerosis. ATA188 has received Fast Track designation from the FDA in both non-active SPMS, for secondary progressive multiple sclerosis, and non-active PPMS, or primary progressive MS populations, in recognition of its potential to address our unmet medical need in these two populations, which represent the vast majority of patients with progressive MS. We plan to continue a productive dialogue with the FDA following the interim analysis of our phase II study. Meanwhile, we continue to make good progress with enrolling the randomized double-blind placebo-controlled EMBOLD study, evaluating the efficacy and safety of ATA188 in patients with progressive MS. Based on alignment with the FDA, our primary endpoint is sustained EDSS improvement at 12 months. We are enrolling patients with non-active SPMS and non-active PPMS, and our current target enrollment of 80 patients is planned to be reached soon after we conduct an interim analysis. Following recent discussion with the FDA, we plan to conduct pivotal phase III studies in both non-active SPMS and non-active PPMS population at the conclusion of this robust phase II study. One study will focus on non-active SPMS, where there are no approved therapies in the U.S. or EU. A separate study will focus on non-active PPMS, where there is only one approved therapy in the U.S. with limited efficacy and none in EU. In parallel, we continue to invest in manufacturing capabilities and differentiated technologies in order to enable clinical supply and biologic-like cost of goods manufactured at commercial scale. Now moving on slide 13 to more detail on the interim analysis. This interim analysis will be performed in Q2 of this year, in Q2 2022. This IA will include efficacy, safety, and biomarker data such as MTR, for magnetization transfer ratio, so we can adjust sample size, if needed to optimize the likelihood of success in this phase II RCT and confirm our development strategy going forward. As it could be a major milestone, reinforcing our conviction in the potential for ATA188, we plan to communicate our decision on next steps for the program, including rationale, while still maintaining the integrity of the study. The key data point at the time of the IA will be EDSS improvement at six months in patients who will have reached this time point. Indeed, based on our phase I data, we know that EDSS improvement at six months is more than 85% predictive of achieving sustained EDSS improvement at 12 months, which is our primary endpoint. As a reminder, we showed 33% EDSS improvement at six months in the high-dose cohort in our phase I study. The result of the IA will determine the sample size necessary to achieve our target conditional power at the end of the study and will inform phase III design and planning. In parallel, we will share the IA data with the FDA to discuss further steps and following strong interest from large pharma companies for ATA188, we also plan to leverage this data to further advance partnering discussion according to our corporate strategy. Now I would like to spend some time to remind you the recent data we presented at ECTRIMS 2021. Starting on slide 14, where we summarize this data from the ongoing phase I open-label extension study, which demonstrate continued safety and tolerability of ATA188, with the longest observed patient having up to 39 months of follow-up. A total of 24 patients enrolled in the study, 18 of whom continued into the open-label extension. Of the 24 patients, nine showed sustained disability improvement and 11 were stable, which means that 20 out of 24 patients achieved sustained disability improvement or were stable. This is remarkable given the expected decline in these patients based on the natural history of progressive MS. Again, 20 out of 24 achieved sustained disease improvement or were stable. Now moving to slide 15, we're showing here clinically significant improvement in some patients treated with ATA188 denoted by the arrows pointing to the left, which indicate more mobility and possible reversal of disease progression. Notably, two patients EDSS scores improved from 6- 4.5, which means that they no longer require the use of a walking aid. Very exciting results. As a reminder, no currently approved therapy in progressive MS show EDSS improvement, only a delay in the progression of the disease. Confirmed EDSS improvement we've seen on phase I are durable for at least 18 months. Now moving to imaging biomarkers on slide 16. ATA188 showed for the first time in non-active progressive MS MTR data suggesting potential remyelination in unenhancing T2 lesions, which are the chronic lesions in progressive MS. First, looking at the right side of the slide 16, changes in MTR were assessed in unenhancing T2 lesions as well as in normal appearing brain tissue, assessed at six months and 12 months, and compared between subjects who showed sustained EDSS improvement and those who did not. Patients with sustained EDSS improvement at any time point showed increase in MTR from baseline in chronic T2 lesions at six months and at 12 months compared to patients who did not. This achieves statistical significance at 12 months and is in contrast to the natural history of MTR changes in PMS, in progressive MS, which is expected to decrease over time. On slide 17, we try to put that in perspective, showing data from the siponimod phase III study in SPMS, showing the expected course for MTR change in normal appearing white matter of progressive MS patients, which is decline or demyelination, as seen in the placebo group of this study. Siponimod shows a smaller decrease in MTR versus placebo, but MTR is still decreasing with treatment with siponimod. In our study, ATA188 uniquely demonstrate potential remyelination based on the relatively large magnitude increase in MTR. Now on slide 18, I would like to conclude this MS part in saying that evidence is building from the medical community that EBV has a direct role in the development of MS, specifically that prior EBV infection is necessary for a patient to develop MS. There are some references here that I encourage you to take a look at, including the last one on EBV potentially promoting the maintenance and expansion of autoreactive memory CD4-positive T cells via molecular mimicry. We should see more published evidence supporting these points in the very near future. Now moving to the third aspect of our strategic priorities and value creation, our allogeneic CAR-T program. This third strategic priority is really around our differentiated next-gen allogeneic CAR-T program on slide 20. Our uniCAR-T platform importantly retains the endogenous TCR, which we believe increase persistence of functional T cells together with partial HLA matching. The insertion of novel 1XX costimulatory domain and PD-1 dominant negative receptor differentiate further our CAR-T platform to have less T cell exhaustion and intrinsic checkpoint blockade to tackle the tumor immunosuppressive environment. On slide 21, you can see that the persistent point is further supported by independent studies, preclinical studies that have shown that the loss of TCR reduce CAR-T T cell persistence and survival in multiple models. Also, knocking out TCR CAR-T cells have been shown to not persist more than three weeks in patients in recent Nature publication. Now on slide 22, we've recently presented encouraging clinical data at ESMO IO last December for our ATA2271 autologous CAR-T product candidate that confirmed the safety and persistence of our armored CAR-T approach. We have now infused a second cohort in the phase I study for ATA2271, and we expect our collaborators at Bayer to submit the IND for allogeneic version, ATA3271, in Q4 of this year. The second allogeneic program we are developing is ATA3219, as you can see on slide 23. We are progressing here with a potential best-in-class allogeneic CAR-T targeting B-cell malignancies with an IND plan in Q4 this year for an improved version of the product. As a reminder, the clinical proof of principle of our approach was confirmed by an investigator-sponsored trial at Memorial Sloan Kettering, where advanced B-cell malignancy patients receive partially HLA-matched EBV CD19 CAR-T cells manufactured from third-party donors, healthy donors. Remarkably, 83% of these ALL, NHL and CLL patients, all with advanced B-cell malignancies, had durable complete response with a median follow-up of 26.9 months, more than two years. We are in fact developing ATA3219 by adding 1XX as an improved costimulatory domain compared to the MSK academic construct. We're also optimizing the cell phenotype, as you can see on the next slide. On slide 24, we have seen recently new evidence in the CAR-T field that show the importance of memory T-cell phenotype for CAR-T efficacy. For example, the Novartis YTB323 CD19 CAR-T data at ASH 2021 highlight the benefit of stemlike, sorry, CAR-T cells. Hence, what we've done is we have modified the ATA3219 manufacturing process to increase memory T-cells, and we have demonstrated more robust in vivo activity in a preclinical model called NALM-6 with such an improved quality version, enhancing our likelihood to develop a true best-in-class in that space. We're also optimizing ATA3219 to further differentiate from other product. On slide 25, you can see that there is still a high unmet medical need to address in DLBCL in particular, that CD19 autologous and allogeneic CAR-T that are currently available or under clinical trials are not fully addressing. Some of the key points of differentiation, first are the safety of EBV CAR-T cells, potential best-in-class efficacy, persistence, and of course, off-the-shelf accessibility. Here we show six months CD19 CAR-T CR data in DLBCL, and you'll notice it's not higher than about 30% across autologous and allogeneic CD19 CAR-T currently being developed. We believe, therefore, that an optimized ATA3219 has the potential to be better. Now, I would like to conclude on slide 26 in summary, in reinstating that tab-cel is on course to be the first-ever allogeneic off-the-shelf T-cell immunotherapy approved in EU this year. In the U.S., we plan to complete the BLA submission for patients with EBV positive PTLD in Q2 2022, with U.S. approval anticipated in first half 2023. For ATA188, where we now have two Fast Track designations, the phase II EMBOLD study interim analysis is planned for Q2 2022 to optimize the likelihood of success and confirm current development strategy. We strongly believe ATA188 has a potential to be a multi-billion dollar opportunity for the company if successful. Our global strategic collaboration for ATA2271 and ATA3271 with Bayer continues to progress well with advancement of the mesothelin partner CAR-T programs, and IND expected in Q4 this year for the allogeneic ATA3271. We continue to advance development of ATA3219, a potential best-in-class therapy for B-cell malignancies that does not require TCR or HLA gene editing. We expect to submit an IND for ATA3219 in Q4 2022. As you can see, we are looking forward to a very exciting year and several value-creating catalysts here at Atara. It will now be my pleasure to take questions. Tessa? Yes, thanks so much Pascal for the presentation. I thought I'd actually start on the MS program, and we did get one, kind of, question in the portal to start, which I thought we could start with, which is what gives you confidence around a real drug effect that you've observed so far based on the phase I data set? I think the question is really around this is no placebo group, single arm study, kind of what are the points that kind of underpin your confidence in the drug? No, I appreciate the question. I think the confidence come from a few aspects of that phase I open-label study, which is around two key aspects. The first one is that this was a dose-ranging type of study where we had four different doses being tested in patients. Not only do we see safety across the dose-ranging and favorable safety here, but we saw a dose-type of dose threshold effect that if you think about the nine patients that had improved disability improvement, sustained improved disability improvement, most of them were treated in the high dose, seven out of the nine. That's something very important to have in mind, that having that difference between low dose and high dose already seen in this phase I study is always a good indicator that there might indeed be a treatment effect. The other aspect that reinforce our confidence is the maintenance of improvement. It's true that when you look at clinical improvement in a disease like multiple sclerosis, you may have patients that have a better day, a better evaluation at one point of time. Having those patients, especially with improvement in EDSS, which is a very, very challenging scale, not only to have one improvement, but to have that confirmed at a second consecutive time point, and then to have that maintained over time, except in one patient, up to 18 months after the confirmed EDSS improvement, this is something very impressive, and we believe that this is not happening in the natural history of the disease, as has been evidenced by multiple publication and clinical experience. The third aspect is the correlation and link between this clinical improvement and this imaging biomarker called MTR, and we presented this data at ECTRIMS a few months ago. Because these clinical improvement that were clear and significant and durable are also showing that these same patients are improved, have an increase in their MTR ratio, which is indicative of potential remyelination. Again, having a dose threshold type of impact, having secondarily a treatment effect that is not only confirmed but sustained with time, and having also the ability to back that up by a biological imaging biomarker, which is MTR, showing potential sign of remyelination, which, by the way, was analyzed in a blinding way. I mean, the team analyzing the MTR didn't know which patient were improving, were not improving. All that reinforce our confidence that we may indeed have a treatment effect, even though it's a small open study with a limited number of patients. Okay. I think you've laid out a framework with which to think about the interim analysis on, I think, slides 13 and 14 of your slides. How should we specifically be thinking about the communication from Atara based on the EDSS interim? Yeah, that's an important aspect of what's going to happen this year. As you know, we have our planned interim analysis in Q2 of this year, so coming relatively shortly. At the time of the IA, we will have access to data that will help us to decide upon the potential extension of the sample size. Do we stay at 80 patients, 40 placebo, 40 active? Or do we increase that further to optimize our chance of success, in fact, to achieve the target conditional power that we have for that study and to have a successful phase II study, robust phase II study. Now, we cannot communicate the details of this interim analysis publicly because that study will still be enrolling patients. We want to preserve the integrity of that study, in particular because we have further discussion planned with the FDA about the study, the status of the product, and how we should look at the development plan for the product. It's very important for the value creation to preserve the integrity of that study. Now, what we can say while preserving the integrity of the study is to not only communicate our decision related to the sample size adjustment or not, but also the rationale for that decision. Again, we will have access to the data of EDSS improvement at six months, and that's extremely predictive of the EDSS improvement at 12 months. As we've seen in our phase I, it was more than 85% predicted. That's really an important data piece of that interim analysis. We also will have to take into context all the other data we'll get at that time of the IA related to imaging biomarker, biological biomarker, other clinical aspect. Based on all that, we'll take the decision. It will be important for us to communicate publicly not only the decision but the rationale, in particular if we decide not to increase or we decide to increase the sample size, why are we deciding so? We cannot be more specific at this stage because of the need to consider multiple type of scenario. We can clearly say that we will be able to communicate the decision and its rationale at the time after having done the IA and having taken our decision. Okay. Are you able to lay out for us, sort of from a kind of broad clinical outcome perspective, when you might consider keeping the study as is, when you might consider expanding the study, things of that nature? Again, the main objective of this interim analysis is to optimize the chance of success of the study. One of the aspect will be once we do this IA, especially looking at EDSS improvement at six months, are we having the right trend here that allows us to really achieve our target conditional power at the end of the study? That's going to be important because we are making assumptions, by definition, when you do a study like that, about what could be the improvement rate in the active group, what could be the improvement rate in the placebo group, based on our phase I data, based on published studies. We have, we believe, a kind of good idea of what we are aiming at. Having access to the IA about the trend and where is that going allows us to potentially adapt the sample size. That's the number one clinical impact would be to adapt the sample size. The other aspect we'll be able to discuss with the FDA around this data, around the status of the product. We already have Fast Track designations. Maybe with such double-blind data we can move to BTD or RMAT designation, so that will allow some discussion. We'll also discuss the development plan, the phase III plan we have, and is it aligned with the data that we are seeing. That will be an important part of the discussion. Thirdly, we'll be able, under confidential agreement, to discuss some of the top line data with potential partners that we've been discussing with for several months now, in terms of the ability to find the right partner for ATU and ATH to move to this very exciting phase of pivotal studies and expansion of the potential indication for that product. Okay, that's helpful. We did have a portal question that just came in. On the interim update, how many patients will we get data on? The interim will be done before having enrolled the patient number 80, because the target enrollment today is 80 patients, and in time to be able to adapt the sample size and therefore potentially continue the enrollment beyond patient 80. We have not disclosed at this stage how many patients are in the interim analysis, but I can tell you that we've already achieved that number of patient enrollment, as well as the necessary time to follow up these patients. They have to be at least six months of follow-up to be able to fully analyze these patients. Some will have been followed for six months following treatment, so for nine months, 12 months, 15, 18, because there have been different type of maturity of the data. We have a sufficient number already enrolled in the study that will be available in Q2 for this interim analysis, with the possibility to have enough patients for confirming our target conditional power in terms of the improvement of EDSS at six months. Okay. I think you've kind of indicated that you're thinking about this program from a strategic perspective, a potential partnering perspective. What are the kind of key factors you could be looking for in a potential partner? You know, I think it sounds like once you have that IA data in hand, that will sort of be the next step towards potentially continuing any dialogue that you've been getting into. Yeah. It's very important for us to not only continue, but accelerate and try to achieve a partnering selection of a partner and a finalization of a partnering agreement following the interim analysis. Why is that so? Because this interim analysis, and could have mentioned that also earlier, is also a key stepping stone to be able to start putting together all the plans for the phase III studies, as well as exploring other indications. Because that IA will give us sufficient efficacy and safety data to be able to start working on the phase III programs in progressive MS, non-active SPMS, non-active PPMS. Also to start working on relapsing-remitting MS and maybe on some other autoimmune disease such as lupus, RA and so on, where there have been a strong association between EBV infection and the disease. Being able to start working on the phase III is to be done together with a selected partner. We want to choose a partner that is ideally a partner that share our views related to the potential of ATA188. We want a partner that really align with us, that if successful, ATA188 has a potential to completely change the therapeutic regimen in MS and maybe in some other autoimmune disease. We want a partner that share our view of a very important product to be developed across multiple indication. We also would like a partner that has the financial and operational capabilities to expand and accelerate with us the development of ATA188 across various indications. Ultimately, finally, and certainly last but not least, a partner that will recognize the full value of ATA188 as being created, and agree with us on the way to share that value going forward in the best interest of Atara shareholders. Yep. Okay. Well, we'll see. We'll stay tuned on that program. In the couple of minutes that we have left, Pascal, I did just wanna ask a couple of other pipeline questions here. I think you kind of covered it in your presentation, but what are the remaining items to completing the U.S. BLA submission for tabelecleucel? And what was the key conclusion with respect to batch comparability by the FDA? The key item to align with the FDA before moving to pre-BLA and BLA submission is really around that comparability between the pivotal product and the intended commercial product. We've made a few very minor manufacturing process changes between pivotal products and commercial product, and since they are minor, you can do analytical comparability. Give you an example, we changed one of the reagents, the location of manufacturing and also to have more GMP compliant reagents. They are really minor changes. We need to be able to agree with the FDA about the comparability between the manufacturing process used in pivotal study and these minor changes of manufacturing process that we implemented to be fully GMP compliant in the commercial product. That's really what we are aiming at with the type B CMC meeting we have already scheduled in Q1 of this year. Once we move out of that, and we agreed with the FDA onto this comparability, we can then do a typical pre-BLA meeting and file the BLA. Now, I would say that what is very important to keep in mind that we already ready to do so. In fact, the fact that we submitted the market authorization application in Europe in November, that has been validated and even that got accelerated assessment, is evidence that we are ready to file. It's really around addressing this particular discussion with the FDA on how to show comparability and showing comparability between the pivotal and commercial manufacturing process, which is, at this stage, the key next step before we can file the BLA, hopefully by the end of Q2 of this year. I think another key question as we approach, a potential approval or approvals here, is how might you price the product given EBV positive PTLD is just kind of the first indication that you're pursuing with tab-cel. You've got a number of other indications in your basket study. How do you think about pricing this product, given those dynamics? Yeah, to start with, when getting approval and being, by the way, in Europe or in the US, we will look at the value that tab-cel is bringing to the patients, to the physicians and medical community, to the healthcare system, and to society. We believe that we already proven through our clinical result that this value is extremely high. Because again, these patients today have no therapy available, no approved therapy, and they unfortunately pass away very fast. The overall survival is just a few weeks to a few months. Here we have a therapy that has been proven time and time again, whether it's in phase II or in phase III, to lead to a very significant level of response, durable response, and long-term overall survival, certainly in the more mature data that we have. The value is there. We will of course and we've done already a lot of pharmacoeconomic analysis to look at the level of financial value when we look at all the benefit that tab-cel could bring to the patient, to the physician, to the healthcare system, and to society. We believe that this value, as I said, significantly high and could lead to potential pricing in line with that value. This is very important for the first indication. Now, for the other indication that we are developing and for which we're expecting first data in 2023, these are all ultra-rare indication, where again there is no approved therapy. We've seen already the type of benefit that tab-cel can bring to this patient, because in each and every of these six additional population for label expansion, we've already presented data, albeit in a small number of patients, but data showing significant efficacy level and, favorable safety. We think that the value, of course, will be depending upon the particular indication. Altogether, we are addressing that with a significant value proposal against no approved therapy in all of these indications, very significant level of response with long-term response, and in those indications that are, potentially fatal, we have this long overall survival. All that is, we believe, justifying a significant value for tab-cel and a price in line with the value. Okay. Then just I'm gonna squeeze a quick one in at the end here. I think you've said initial data from the basket study in 2023, do you have a sense of what cohort or cohorts that could come from? Yes, we already have some sense about it. I think it's not surprising that the two cohorts that have the most patients today in general in the population that we are targeting are the primary immunodeficiency LPD and acquired immunodeficiency LPDs. Especially the acquired immunodeficiency LPDs or for lymphoproliferative disorders in people that are immunocompromised because of either the treatment or their disease. This is a large number of patients, so these are clearly the cohorts that are enrolling faster in our study. That's where we should expect the first data to come from. Okay, great. Well, thank you, Pascal, for what I thought was a productive discussion. We appreciate you being part of the conference. Thanks to all of our listeners as well for joining. We hope you have a great rest of the week, great rest of the conference. Thank you, Tessa, and thank you, JP Morgan, and we are keen to have an exciting 2022 years with a lot of value creation catalyst for shareholders. Thank you.