Good afternoon, everyone. Thank you for joining this session for the GSK Fireside Chat. For those of you who do not know me, I am Sarita, European Pharma Equity Analyst at Morgan Stanley, and I am very pleased to have Hesham with us today, who heads up oncology at GSK. Thank you very much for joining us. Before we get started, just some housekeeping, which I am sure you have all heard, but please note that this presentation is for MS institutional clients and employees. For important disclosures, please see the Morgan Stanley research disclosure website, sorry, at www.morganstanley.com/researchdisclosures. With that, let us get started. Perhaps we can start with the overall oncology strategy. At the Accelerate Growth CMD, you laid out a much broader opportunity across lung, prostate, GI, gynecological cancers, and then significant late-stage investment. When you think about oncology today, where do you still see the genuine gaps? Are there areas of oncology that you have deliberately chosen not to go into, and where are the areas of interest moving forward? Yeah. Well, Sarita, first of all, thank you very much for the kind invite. It is great to be with everyone today. It is great to be at this conference as well, too. I know I was here last year as well, too, so fantastic. With that in mind, probably just reflecting a little bit on the past four years of oncology at GSK, I think everyone is well aware, of course, that we had stepped away in 2014. We have come back. But I think probably if you ask me what was the secret recipe in all this, it is focus. It is focus, it is being very methodical in terms of how we have approached the rebuild that has taken so far with GSK. It is not often that a big pharma company steps away from the field of oncology and then tries to reenter it, and then when it reenters it starts to have a lot of great success moving forward as well, too. But I think it was probably owing to a number of key variables. First, we really tried, to your point, focus on disease areas where we felt like the unmet need continues to exist and where we can establish key capabilities across talent, disease knowledge, and of course, better characterizing the biology of the disease as well, too, to help drive discovery research efforts, but also a translational focus as well, too. Let alone the fact that not only did we rebuild these capabilities in these key disease areas, but also we reestablished our medical affairs presence and commercialization efforts as well, too. We started first in key heme malignancies, so across multiple myeloma, myelofibrosis. I think everyone's well aware, of course, belantamab mafodotin and momelotinib, or Ojjaara, has been the key pillars in heme malignancies for us, but also building on the success that we've had with Zejula and, of course, dostarlimab as well, Jemperli, across ovarian and endometrial cancer, respectively, in gynecological malignancies. From there, we started to continue to add additional tumor types that we felt like, again, where our capabilities could be built, and the depth of experience could be developed, and then where we felt like the unmet need continues to exist. Now that has expanded to thoracic malignancies, lung, and head and neck, GI malignancies with a focus emphasis on colorectal cancer, again, building on the success that we've had with Jemperli. Then finally now starting to move into prostate cancer as well, too. Certainly, we just are starting to initiate three phase III studies with our B7-H3 or Ris-Rez antibody drug conjugate. We're also building a portfolio of assets that are giving us a good critical mass across different therapeutic modalities in prostate cancer as well, too. This has all been, I would probably say, a mixture of organic growth, so in-house portfolio discovery research efforts, but also inorganic growth. A lot of business development. You've seen some of the recent BD deals that we've done. I think probably Nuvalent is the most notable. Then at the same point in time, just this morning, we announced another licensing for a tri-specific immune cell engager in multiple myeloma as well. Perfect. You touched on BD M&A. Nuvalent was perhaps a much larger later-stage transaction than we've seen recently in oncology for GSK. Should we think about Nuvalent as a one-off opportunity, or has that changed the size that you would look at in oncology? Perhaps because you mentioned it, you can touch on the T-cell deal from this morning, too. Yeah. I think it's a really key question. Probably over the past few years, if you asked me about what is the philosophy that we've had around our business development activities in oncology specifically, I would say first and foremost, there is a framework that we follow. The framework goes along the lines of the following. One, is the licensing or acquisition going to address a key unmet need that we feel like is very unique at this time? That's the first point. The second really is around the medicine or the medicines that are involved, and specifically with regards to, are they differentiated in the context of their medicinal design, in terms of their mechanism of action, in terms of the pharmacology and the properties that they offer? Do they provide what is the potential for a best-in-class profile? The third, is there preliminary clinical data that exists that gives us additional confidence in the probability of technical success of the assets? The fourth, of course, does it align to key strategic disease areas of interest for GSK and where we have these capabilities that have been developed across R&D, medical, and commercial? When I think about Nuvalent, certainly it's not just a singular asset. I think we have to think about it's not a one-asset deal, it's actually two key assets, and then there's also a discovery pipeline of programs as well. The two key assets, of course, are neladalkib, which is a fourth-generation ALK inhibitor with a best-in-class potential. Then, of course, also zidesamtinib or Jideytro, which was just approved in July of this year in ROS1 mutated patients as well, or ROS1 positive patients as well. Again, two assets, I think the deal size quite large, but we've also done deals across the board. Everything that has ranged from GBP 1 billion- GBP 2 billion. For example, the Sierra Oncology acquisition for momelotinib was about maybe GBP 2 billion. The IDRx acquisition for velzatinib was about maybe GBP 2 billion. We've done larger deals. I think that the bottom line really is it depends on what type of synergy complementarity and the profile of the deal itself and how it adds to our existing portfolio. I think if you look at Nuvalent, for example, I think it probably now gives us that piece that helps us form what is a franchise in lung cancer. Two different assets, highly differentiated, best in cost potential. Then we have our Ris-Rez B7-H3 ADC, which we actually just presented, certainly, through our partners, phase III data for, at World Conference on Lung Cancer. We've got a lung franchise that's emerging as well for us in that context as well. Moving forward, what do I expect in terms of deals? I think probably, across the range of everything that we've done from either licensing, like this morning, of course, this tri-specific T-cell engager and multiple myeloma, to acquisitions that we've done, like IDRx and certainly Sierra Oncology. When it happens, and it depends, certainly larger deals could exist if they present themselves as well. Okay. Very clear. Thank you. I do want to get into Nuvalent and B7-H3, as you mentioned. But before, when we think about 2031 sales and the overall GSK target for over GBP 40 billion of sales, and I appreciate you're not commercial, but maybe thinking about it in a different way, what are the two or three most important oncology assets to achieving that target, and where do you have the most conviction? Yeah. Probably it is an interesting, for me, time to reflect on the progress that we have made, but also where the pipeline is at right now as well, too. I think if you look at it, four years ago, we did not have many medicines approved. We have got five medicines approved now, a sixth to be approved by the end of the year, which is, of course, neladalkib has a PDUFA date in November of this year. But also three additional assets, B7-H3, B7-H4, and velzatinib, that are likely to hopefully make it to the market by the 2028, 2029 timeframe as well, too. Biggest opportunities, I think, no doubt, B7-H3 is a key asset, just owing to its broad expression profile across a number of different solid tumors. So that includes, of course, thoracic malignancies, GI malignancies, GU malignancies like prostate cancer as well, too. We oftentimes refer to it as a pipeline and an asset, right? Just given how broad its applicability is. B7-H4, Mo-Rez as well, too, especially in gynecologic malignancies, velzatinib and GIST, and then probably there, people might look at GIST at face value as a relatively more orphan patient segment. But I think duration of therapy is really important, and I think when we look at, for example, imatinib or Gleevec now, and the fact that it delivers probably somewhere between 28- 32 months, or 33 months, a median PFS in frontline GIST, you are looking for a meaningful improvement over that. So duration of therapy is a critical element, similar to probably how we look at the Nuvalent assets as well, too. Nela and zidesamtinib. If we are thinking about ROS1 positive patients, about 2% of lung cancer, ALK positive patients, about 4% of lung cancer. But duration of therapy is very critical, especially if patients are on treatment for several years. So I think these are all assets that are going to be contributing to those 2031 ambitions. And of course, along with Blenrep, as we think about the future of newly diagnosed patients, DREAMM-10 and frontline multiple myeloma as well. Okay. Lots going on. Maybe we can start with Nuvalent and the data over the weekend for Jideytro, and apologies for my pronunciation, in first-line ROS1. The data is still perhaps relatively early in a small number of patients, 94 patients. So help us understand where we are with filing for first line. What else do you need to see to kind of get comfortable with the regulatory path? Yeah. Well, the data was actually presented at the plenary session yesterday morning in Seoul. I just got in yesterday night into New York. Quite a warm reception to the data, quite robust, spectacular, I would say, certainly for ROS1 positive patients as well, too, in this first-line TKI naive, non-small cell lung cancer patient population. 94 patients, 94% objective response rate. In terms of at least the durability, we are seeing a PFS landmark at 12 months of about maybe 90%. Certainly a duration of response landmark at 12 months of 86%, so quite durable, quite strong treatment effect, and very clinically relevant. Then, of course, the medicine was designed to have these brain-penetrant properties, and in that subset of patients that had brain metastases, and typically in these ROS1 and ALK positive patients, about maybe 30%-50% of patients typically develop brain metastases. We saw 100% response rate in terms of intracranial response, which is probably, again, very important for patients. Overall, a lot of confidence, very strong support for how we feel about the drug at this stage, especially when you think about comparisons as they are made to, for example, third-generation TKIs as well, too. We are still planning on filing in Q4 before the end of the year. One point to also highlight in that regard. Of course, I think it is well established, at least from a regulatory standpoint, that given the orphan nature and the prevalence of the disease, of course, as well, too. We have seen single-arm studies and single-arm data sets serve as pivotal and certainly registrational data sets in this first-line TKI naive ROS1 positive patient population. So, we feel very comfortable with the approach that we are taking from a regulatory standpoint as well. Okay. Perfect. Very clear. Thank you. When we think about neladalkib in the first-line ALK lung cancer setting, lorlatinib has set a very high bar for efficacy and particularly for durability, brain control. ALKAZAR, the frontline trial, is versus ALECENSA. Is it meaningful enough to show superiority to ALECENSA, or would you need to show, at least on a cross trial, something lorlatinib-like to change practice? Well, I think we have to look at where the uptake of these medicines is right now. I think if you look at the most recent market data and the uptake and the usage and physician usage of these drugs, we are actually seeing about maybe 45% use of alectinib in the frontline setting, with about maybe 35% of patients use of lorlatinib. So alectinib is quite still a relevant control arm in that frontline setting as well, too, and that is why the study was actually designed that way. Now, I think if we look at other third-generation TKIs and the comparisons that were made, they were actually made to first-generation TKIs, to crizotinib. I think that is something to just kind of bear in mind and take into account as well, too, in their pivotal studies. The data, at least certainly is, at least in that second-line TKI-pretreated patient population, quite strong, and probably also gets at the fact that neladalkib, similar to alectinib, was very much from a medicinal chemistry design, designed to address not only the single ALK mutations, but also the compound ALK resistance mutations as well, along with, of course, its brain-penetrant activity. From that standpoint, I think we'll be able to see very clearly, hopefully, the treatment effect over alectinib. At the same point in time, probably something to highlight, of course, the data that's been generated and presented for neladalkib in this first-line TKI-naïve patient population as well. Looking at, of course, not only the objective response rates, which is quite high, but also the duration of response at 12 months being at 91% versus 70% with the third-generation TKIs as well. So we expect to see that separation hopefully happen early between certainly neladalkib and alectinib in that phase III study. By the way, the recruitment in that trial is going quite well. Okay. Could you remind us when the trial is due to read out? Is there potential for the trial to read out earlier at interim? Could you give some color on when that could perhaps be? Yeah, I think I would probably say that it's difficult to tell when the data would read out because there are a number of different variables that go into that. First, of course, is the, I would say, one, the recruitment rate is very critical. So I think that plays a key role. The second, of course, is the event rate and how quickly events actually occur. I think bear in mind, of course, that in this instance, we're going up against a second-generation TKI, not a first-generation TKI. The third, of course, is when does that separation happen between the two? I was just referring to the duration of response and already seeing, at least based on cross-study comparisons and, of course, with all the caveats that they provide. We're hoping to see that separation occur early. And of course, as is the case with any clinical trial, oftentimes there are different levers to be able to incorporate into them, including, of course, looking at potentially interim analyses that hopefully can provide additional insight into overwhelming treatment effects as well. Very clear. You touched on duration of response. These patients stay on therapy for a long time. How should we think about the tolerability profile with neladalkib, particularly the liver piece versus some of the neurological metabolic side effects that we see with other TKIs? Yeah. The experience that we've had to date, at least looking at the, I would say, the liver transaminitis that's been observed with neladalkib, is that these are oftentimes quite asymptomatic, transient, and quite reversible as well, too, oftentimes reversing within a span of about maybe two weeks or so. Certainly from a TKI perspective, from a thoracic oncology standpoint, and especially in this driver mutation segment of patients, physicians are oftentimes quite comfortable, of course, with how they manage these types of transaminitis cases. Liver function tests are typically conducted for patients when they come in as part of their more standard or routine, I would say, battery of labs that are conducted with the visits that they have. Generally from that standpoint, we don't have much of a, I would say, probably concern in terms of having confidence in their reversibility, their monitoring, and the transient nature that they have as well, too, and the fact that they're asymptomatic as well. Like I said, the majority of these events have manifested in that way. Perfect. Perhaps we can move on to Ris-Rez, the B7-H3. You presented some exciting data over the weekend in relapsed small cell lung cancer. Perhaps for the benefit of everyone in the room, it would be great to hear your thoughts on the dataset. Yeah. I would say, again, quite robust data for the B7-H3 ADC Ris-Rez at World Lung from our partners, Hansoh Pharma. Phase III data in second-line small cell lung cancer, looking at Ris-Rez versus topotecan. The data quite compelling and quite internally consistent, which I think is important. So hazard ratio of 0.46 for overall survival, hazard ratio of 0.33 for PFS, and probably close to five times improvement in objective response rate, along with the durability, of course, as well, too. That's quite probably notable as well, too, including the median OS that was observed on the Ris-Rez arm, which was about maybe 18 and a half months, which is quite, I would say, important as we look at the benchmarks that have been previously set in that second-line space including with immune cell engagers, where we see about maybe a 13 and a half month median OS, and with other B7-H3 ADCs, which ranged around between 12- 13 months. So again, quite a robust data set and certainly an important inflection point for the Ris-Rez development program moving forward as well. Amazing. This was a China trial, so how confident are you that the results will hold in a more global population, particularly given some of the other things we saw at World Lung with EVOKE-03 being better in China patients? So how should we think about that? Yeah Across the global population? I think there's always nuance as to how we think about these comparisons. I think probably for us at least, as we think about ARTEMIS-008, there's probably two or three key variables that we have to take into account. The first is, I think you have to look at the behavior of certain, I would say, elements of the study itself. For example, the control arm of the trial. In this instance, the topotecan control arm, it demonstrated a median overall survival of about maybe 10.3 months. Let's put that into context with regards to how the control arms of other phase III studies globally have looked when topotecan has been used in this disease setting. Probably the closest or most recent analog is the study from lurbinectedin, which is the LAGOON phase III trial, which actually didn't meet its primary endpoint, didn't demonstrate that lurbinectedin was better than topotecan. But the control arm on that study actually demonstrated a median overall survival of 10.6 months. So it is consistent. The control arm behaves in a very consistent way with at least the global data set from another phase III study. The second I would probably say is, I think we are very fortunate to be able to have the ability to look at data sets from Hansoh in real time, but also our own internal global development program, the GSK-conducted global development program as well, too. Of course, we have phase I, II data as well, too, in the small cell lung cancer setting, in the second-line patient population. We've seen at least the data published from Hansoh, their phase I, II data at World Conference on Lung Cancer a couple of years ago as well, too. I can tell you, without disclosing the data, the data is very consistent on the GSK side as well, too. So that gives us additional confidence, at least in terms of the translatability of the experience in China relative to a global population in the GSK development program. Stay tuned, you'll see that data in several weeks time at a key scientific congress as well, too. Then finally, probably the third component that gives us, of course, additional confidence is the robustness of the data, as I'd alluded to as well, too earlier. Oftentimes, if you see one data point be positive, but there are outliers in the additional data points or in the subgroup analyses, it makes you wonder whether the treatment effect is truly consistent or not. I think when you looked at a number of different primary and secondary endpoints, the data is highly consistent, and across different subgroups is also very consistent as well. All three points probably give us additional confidence and belief that the results are certainly more extrapolatable to a global patient population, including our own development program. We actually have an ongoing second-line phase III study, which is actually recruiting quite well in this second-line small cell lung cancer population. Thank you. You talked to the kind of consistency, the robustness of the data, and perhaps not for the U.S., but could the China-only data be sufficient for an approval ex-U.S.? Yeah, I think it's a great question. What I would say is, I think we've seen examples in the past where PD-1 inhibitors that have phase III studies that have been conducted in China support registration in other countries, markets, and regions, including Europe. I think for us, we just have to evaluate the data sets, look at any potential options that might exist, and explore different strategies as part of our regulatory thinking as well. You mentioned that several B7-H3s in development. What underpins the confidence in Ris-Rez being best in class? Perhaps you can touch on the rates of ILD versus some of your competitors, too. Yeah. Well, first of all, I would say, we have been executing at pace. That is probably the headline that I want to leave everyone with is, the pace and the acceleration that is taking place on this program has been quite, I would say, fast. We have actually just recruited and treated our 1,000th patient on our global development program as GSK, which is fantastic and phenomenal. We are initiating five phase III studies. Two, of course, in small cell lung cancer, second-line small cell lung cancer, which is ongoing. First line small cell lung cancer, forthcoming. Then three pivotal studies across different lines of therapy in prostate cancer. So, one in late-line metastatic castrate-resistant prostate cancer, another head-to-head against chemo in a chemo-naive metastatic castrate-resistant prostate cancer, and then another in a metastatic hormone-sensitive prostate cancer population. In terms of the ILD rates, I would say we have data from our global development program that I will actually be presenting at a key scientific congress in a few weeks' time, which I think we will probably find very interesting in terms of the rates and the incidents of ILD that have been observed in our global development program. It may be unique relative to other linker payload platforms that exist in the class as well, too. Probably, I would say a data point, a reference point to highlight is, of course, our B7-H4 ADC actually uses the same linker and payload as well. We presented preliminary data on ILD at SGO from that program, and it showed only a 3% incidence of ILD, the majority of the events all being of low grade as well, too. Perfect. Before we get into the B7-H4, you mentioned the broad prostate cancer development. What gives you confidence that you can kind of take a B7-H3 or ADC from the metastatic setting into the more chemo-naive sensitive setting? Yeah. I think looking at, of course, the data that has been presented already publicly by Hansoh. We have seen a 37% confirmed objective response rate in metastatic castrate-resistant prostate cancer. That response rate was not interacting in any way, whether it be with prior chemotherapy or no prior chemotherapy as well, too, very consistent, which I think is important. The second, of course, is we are actually generating our own data set in our own global development program. Again, we have the ability to be able to view both of these data sets, look at their consistency as well, too, which gives us additional confidence. Stay tuned, that data set will probably be presented at a key scientific congress in the first half of 2028, in prostate cancer as well, too. We feel very comfortable with being able to take on an ambitious and initiate an ambitious program in prostate cancer moving forward. Perfect. When we think about Mo-Rez, the B7-H4 ADC, it's a similar question, in a way. We've seen encouraging data in ovarian cancer, but there are a lot of B7-H4s in development. What differentiates Mo-Rez and what's kind of underpinning the confidence in it being best in class? Sarita, I think that's an important question, and first and foremost, no doubt there's a number of different ADCs emerging in this gynecologic oncology space. But our confidence, first and foremost, in the linker and the payload technology, which has been established and based on the Hansoh Pharma experience, our experience across both Ris-Rez and Mo-Rez is important. The second, I think we've seen already the preliminary data that was presented at SGO, 67% confirmed objective response rate at the 5.8 mg per kg dose in platinum-resistant ovarian cancer, and a 67% objective response rate across the 4.8 mg per kg dose level in second-line endometrial cancer as well, too. That is probably, I would say, in the top tier of numerical response rates that have been observed across the class of ADCs in gynecologic malignancies, which I think is important and relevant. The third really is, execution is one component, speed is one component, but also translational strategy becomes very critical. Although we haven't necessarily seen any interactions between B7-H4 or antigen expression and clinical activity, we see broad activity across different antigen expression levels. We're also continuing to look into biomarkers, and I think what we're learning with ADCs is certainly, we're moving much more from univariate antigen expression focus to much more multivariate biomarkers, including, of course, looking at the sensitivity of the tumor to the linker and the payload within the tumor microenvironment. Which I think now, again, makes us think about not only oncology, but ADCs through a different lens, and could potentially, of course, be important in terms of further optimizing the treatment effect and the benefit risk overall. Very clear. You touched on B7-H4 expression, and I believe in endometrial cancer, it was kind of widespread efficacy irrespective of expression. Some of your competitors, for example, AstraZeneca with [inaudible], are looking at a biomarker-specific approach. Is B7-H3 just not the right biomarker, or is there something specific to your asset, which means it's kind of more broad? To be honest, I think it's a question I probably can't comment much on the molecules for other sponsors and their experience with it. But I think they see something in their data that could be indicative, potentially, of an interaction between B7-H4 expression and treatment effect. For us, it's not something that we've seen so far, specifically in our platinum-resistant ovarian cancer dataset either as well, too. But we're looking, like I said, at probably more multivariate biomarkers as a means of, again, further enhancing the treatment effect that we've already observed as well, too. I think it's important, because in a space where we're going to have a number of different competitors, I don't think we can purely rely on just looking at numerical values of response rate. When you talk to physicians, when you talk to experts in the gynecologic oncology space, the two key drivers for how they're thinking about how they'll manage patient care moving forward, and especially with the presence of multiple ADCs directed towards different targets, whether it be folate receptor alpha, whether it be B7-H4, whether it be Trop-2. One, of course, is how much can you optimize the efficacy? Then two, what does the safety and tolerability look like? We've seen that certain antigens with ADCs have unique toxicities like stomatitis, which can become quite a big challenge. Others, for example, ocular toxicity in that gynecologic oncology space, and then others as well too, certainly, looking at peripheral neuropathy and certain types of unique toxicities. Perfect. Perhaps taking a step back, you have a lot of exciting mechanisms already in your portfolio, ALK, ROS1, the ADCs. Is there a particular mechanism emerging, whether it be PD-L1, VEGF, pan-RAS, et cetera, that you think is particularly exciting that GSK is not currently operating in? Yeah. I don't know if there's one singular kind of mechanism, Sarita, you mentioned a few of them as well. Interestingly, we just did a deal, of course, a couple weeks ago for probably what is a unique first-in-class antibody-targeted therapy conjugate in this RAS space. Some are taking, of course, this pan-RAS approach. Others are taking a pan-KRAS or more KRAS selective approach. We actually basically looked at evaluating a more unique approach, which is basically pairing an EGFR-targeting antibody with a pan-KRAS payload to help drive a much more targeted and specific delivery of the mechanism through the internalization of the receptor as well. We think that there are ways to look for this best-in-class, sometimes first-in-class potential, if you understand the biology well enough, and then you also find the right technology to pair with it as well. For us, I think, the RAS space is one element. I think you've seen how we've come into the ADCs as well. But also even these driver mutation segments. It's very important. I think about, for example, the [inaudible] data and say, "Wow, you can actually more than double the CR rates in these first-line TKI naive patient segments, 15% CR rate," and with the hope, of course, that these are durable and potentially could drive to more curative states. I think that's fantastic. For example, with neladalkib, if you can design an asset that is much more selective, that spares patients the metabolic changes and effects, that actually gets away from the neurocognitive effects and CNS effects that other medicines in this space have, so that it helps improve the tolerability burden for patients. That's what we're really trying to do. We're really trying to target these best-in-class medicines. I think hopefully that will be important for patients moving forward. Perfect. In the last couple of minutes, is there something you'd like to highlight in the oncology portfolio that you think we should be focused on that we're not? Or is there something about oncology at GSK you think the market is missing? Yeah. I would say maybe two or three things. I will start out first and say, wow, what a difference do four years make, right? I would say the journey that a big pharma company has taken from stepping away from oncology and then coming back into it and then having success. There is actually, just for those that might be interested, there is a Yale oncology conference taking place on November 9th and 10th in Connecticut. I am actually going to be giving a keynote, and the keynote actually will focus on some of the key learnings from this journey, of a case study for a big pharma coming into oncology and what has been done well to get us the success that we have achieved to date. But we have now five approved medicines, six by the end of the year, and then three more by 2029, so nine. That is quite a journey in only a few years' time. The second, I think I would probably say stay tuned for B7-H3, B7-H4, velzatinib, and then, of course, neladalkib in first-line TKI-naive patients. I mentioned that we have made a lot of great progress with the first-line study, the ALKAZAR study. Maybe this is something that I will share now. We are actually probably at about, we said that maybe the growth event we were at maybe about 35% recruited. We are at 47% recruited. This is only just in a span of about maybe four or five weeks. So we are moving at pace. The execution is quite, I would probably say, methodical and excellent. The third really is choices that we make. Choices matter strategically, what you do, but also what you do not do. Strategy is about actually both. I think for us, we have been disciplined in what we do and what we do not do. I think that is helping us succeed as we move forward now, and I am looking forward certainly to what the next 12- 24 months will bring. Amazing. Thank you so much, Hesham.