Good morning. Welcome to day four and the final day of the 40th JP Morgan Healthcare Conference. My name is David Choi, and I'm an associate in the JP Morgan Healthcare Investment Banking group. Before I introduce you to our next company, I'd like to draw your attention to the blue box at the bottom of your web page. If you could submit all your questions through that link, it would be much appreciated. With that, I'm pleased to introduce you to NGM Biopharmaceuticals. We have David Woodhouse, CEO of the company, on behalf of the company. With that, over to you, David. This is David. Thank you all for joining the presentation this morning. At NGM, we're explorers on the frontier of life-changing science, and our vision is to make lasting scientific contributions that improve human life. Today, I'm looking forward to giving you an overview of the company and what we're looking forward to this year. If you take one thing away from today, it is that our platform and pipeline is really hitting an inflection in 2022, and I'm excited to share with you the important elements that we think will drive that. As a reminder, I will be making forward-looking statements during my presentation today. Please refer to our SEC filings for more information. 2022 is poised to be the most event-filled year for us yet at NGM with multiple catalysts on deck across our deep pipeline of clinical-stage assets. We're pleased to share new clinical data from three of our programs in 2022. Topline data from our phase II study with NGM621 in geographic atrophy, and interim phase I clinical data from two of our oncology programs, NGM707 and NGM120. We're preparing to advance two of our other programs into the clinic in the first half of the year, NGM831 and NGM438, both in oncology. We're imminently completing enrollment into ALPINE 4, our phase IIb trial with aldafermin in cirrhotic NASH to be set up for data in the first half of next year with that program. Merck continues to make progress advancing MK-3655 through phase IIb development in non-cirrhotic NASH. All of these programs stem from our biologics discovery engine that is at the heart of the company. The quantity of milestones that we're looking forward to in 2022 and breadth of disease areas that our programs cover, both of which we think are unique to a biotech of our stage, speak to the robustness of our discovery engine. In addition to the milestones on the page, our research labs are continually generating new therapeutic candidates at a pace of about one new IND per year. How does our discovery engine work, and what is the common thread between our diverse preclinical programs? Well, as depicted on this slide on the far left, we start with interrogating biology. We are experts at exploring novel disease pathways and mechanisms behind disease, and we deploy a variety of strategies and tools to do that. In tandem, as shown in the figure on the right, we pair those insights with industry-leading expertise in protein engineering that allows us to develop tools to probe the pathways we are studying and ultimately generate product candidates that are intended to help reverse or slow a disease. Implicit in this approach is having a very talented scientific team, and that is truly our secret sauce, the people behind the platform. I'm really proud of the numbers you see on the right of the slide. These statistics reflect how productive this discovery engine has been over the several years we've been operating it. We have seven disclosed programs across three therapeutic areas, with five currently in the clinic and the rest entering the clinic in the first half of this year. Four of our candidates are actually in phase II trials, which we all know are key value creating priority programs. For that, let's take a look under the hood of our discovery engine by giving a few examples tying our approach to our pipeline. The biology capabilities emphasize strengths in human genetics, high-throughput in vivo screening, and receptor ligand de-orphanization. We also have protein engineering expertise in a variety of biologics, including all types of antibodies. Each of our programs in our pipeline, summarized on the right, have emerged from combining different components of these capabilities on the frontier of new biology. To call out a few examples, our NGM120 program stems from work from a particularly powerful hormone called GDF-15 that, when elevated, is associated with poor prognosis for cancer patients. Our team was the first to identify the receptor for GDF-15 and generated a high-affinity antibody to block that receptor and hopefully help cancer patients fight their disease. Aldafermin and MK-3655 stem from high-throughput in vivo screening we did on factors elevated after gastric bypass surgery to drive improvements in metabolic syndrome. Our protein engineering capabilities then leveraged those findings to create optimized biologics to mimic the activity of those factors we have identified. Those programs we think of as wave one from our discovery engine. Today, I'm gonna focus on several programs that have emerged from our ongoing evolution of the platform that emphasizes human genetics and systems biology research applied to cancer and retinal diseases. Beyond the specifics of how we've translated biological insights to product candidates, the important takeaway is that our approach is repeatable. We have successfully applied it across varying and complex biology to date, and we'll continue to do so going forward. Turning to our pipeline, we think about it in two distinct segments. Our wholly owned oncology portfolio, where we have the ability to demonstrate proof of concept early in clinical development and advance programs relatively rapidly. Our non-oncology programs, where we develop high-potential therapies to the point of partnership and leverage late-stage development capabilities of partners while retaining meaningful backend economics. Our retinal portfolio and NASH portfolio fall in this latter category. Establishing these two segments of strategic intent for our pipeline was the primary motivation for us last year when we renegotiated our collaboration with Merck. Today, I'm gonna focus upon our NGM621 program for geographic atrophy and our portfolio of myeloid reprogramming candidates development for the treatment of solid tumors. Let's start by walking through the NGM621 program. We're developing NGM621 for the treatment of an advanced form of dry age-related macular degeneration, or dry AMD, called geographic atrophy. This image on the right is what patients suffering from this disease experience. Geographic atrophy, or GA, is a degeneration of photoreceptors in the retina that causes progressive and irreversible vision loss. It impacts not only a person's sight, but of course, their mobility and independence later in life. There are about 1 million patients in The U.S. and 5 million worldwide with geographic atrophy. Unlike the wet form of AMD, there are no approved therapies for the dry form that underlies GA. We're at an exciting time in GA development area, though, since after many years of target exploration in the industry, we finally have had a few clinical data sets in the field show that complement inhibition, in particular complement C3 inhibition, is able to slow progression of this disease. For those of you that have followed the development of the wet AMD treatment landscape over the last decade, we think dry AMD and GA will develop in a very similar fashion. The first few drugs approved to establish the proof of mechanism. The ultimate category leaders become the later entrants that have optimized attributes. We'll now turn to why we are taking the approach we are with NGM621 and what advantages we think it brings to the treatment landscape that can make it a category leader. The pathology of GA is not entirely understood, yet there's genetic evidence and histopathological evidence for complement playing a role in the development and progression of the disease. In this chart on the left, each of these tall spikes that have red arrows on top represent an association of genetic variations in components of the complement cascade and the likelihood of developing GA. On the right, it shows complement deposited at the location of photoreceptor degeneration in these scans of retinas from patients suffering from the disease. How do we take these biological insights and others and turn them into a drug candidate? Well, our approach is to target complement C3 specifically and block its activity with a high-affinity antibody. We are the only company in the clinic with a monoclonal antibody inhibiting complement C3. By virtue of it being an antibody, it has a hydrodynamic radius that is relatively large and helps it persist in the eye for a prolonged time without the need for [circulation]. The power of blocking complement C3 is that it is a single target that can deactivate the entire complement system. Whereas any other target within the cascade may still allow some activity of the system, effectively only capable of partial inhibition. As I mentioned earlier, there's convincing clinical data in the development landscape that demonstrates its effect in slowing progression of the disease. What are the characteristics in NGM621 we think could drive differentiation in the landscape? There are three ways to improve and benefit the patients. First is potency. The chart on the left shows the standard functional assay of inhibition of two major pathways of the complement cascade. You can see that NGM621 blocks both pathways at a similar low nanomolar affinity, and this potency compares favorably to other molecules in the landscape. We think potency could translate to improved efficacy and/or less frequent dosing. Next is convenience. We think NGM621 has the potential for every other month rather than monthly dosing. With intravitreal injections, this could be a significant advantage. The chart in the middle is PK modeling from our phase I study that suggests greater than 90% inhibition of C3 is well beyond 30 days to nearly 60 days. Finally, potential safety advantages. Certain competing molecules have observed an increased number of wet AMD-like conversions in their clinical trials in GA patients. We don't expect to see that with our drugs. On the right of the slide, we show a preclinical model of wet AMD. NGM621 does not worsen vascular leakage or angiogenesis, and may actually suppress it. By virtue of not having to titrate NGM621, we think this could help lessen the development of the activated form of AMD. Our market research suggests even small differences in the percentage of patients who develop wet AMD could be very meaningful in informing which drug practitioners prefer to use. As we've learned from the wet AMD marketplace, any one of these improvements could meaningfully differentiate NGM621 and position it well to become the treatment of choice for GA. Our ongoing phase II study with NGM621, called CATALINA, is reading out in the fourth quarter, and it's designed to provide further support for the sources of differentiation for NGM621 that I just walked you through. We announced in July of last year that we had completed enrollment for 320 patients stratified among four arms testing monthly and every other month intravitreal dosing of NGM621 versus sham arms. The primary endpoint is the rate of change of geographic atrophy lesions over a 52-week period. We expect the trial has the potential to be considered a pivotal trial if statistical significance is achieved. NGM621 is subject to our collaboration with Merck. As I mentioned, we expect to report top-line data from the trial in the fourth quarter, and this will also trigger Merck's option to license the program in addition to other undisclosed preclinical programs that we have in the retinal disease area. If they do decide to option the program, we have an opportunity to retain up to half the economics through a cost profit arrangement. Now let's turn our attention to another area of our pipeline that represents a collection of programs in a new area of immuno-oncology that we think is positioned to be the next wave of important new additions to the cancer treatment arsenal. Five years ago, we decided to focus a portion of our discovery engine on next-generation targets in oncology. We saw the power of mobilizing a patient's own immune system to fight cancer. We strongly believed that there were targets that hadn't been explored that could drive even better responses. We all know that PD-1 inhibitors and T cell checkpoint inhibitors generally have been transformational in cancer treatment, but more is needed. What we're looking here on the left of this slide is that not all patients are responsive to PD-1 inhibitors, leaving overall about 70%-80% of patients not benefiting from this class of drugs. The data we're showing here is specifically in non-small cell lung cancer patients. On the right side of the slide, many patients that initially respond to T cell checkpoint inhibitors become resistant and end up progressing. We directed our research towards how we could drive a broader and deeper response for cancer patients in this context and hone in on the supportive immune cells, generally referred to as myeloid cells, that we believe represent the second checkpoint solid tumors use to avoid detection and attack. Let's take a look at the evidence that myeloid cells may be important participants in driving immune response to tumors. The darker green line on the far left here that falls off a cliff in these survival curves are patients that have high levels of macrophages, a key type of myeloid cell, and low levels of T cells associated with a tumor. The takeaway from these data and others is that myeloid cells and T cells act in concert to drive antitumor immunity. Just overcoming the T cell checkpoint with an anti-PD-1 does drive response in some patients, but others with cold tumors that don't respond are believed to have a population of macrophages and other myeloid cells in the tumor microenvironment, which can act as a second checkpoint on the immune system that prevents more robust antitumor responses. When we looked at what receptors are overexpressed in patients that don't respond to T cell checkpoint inhibitors, the four receptors on the right of the slide that are primarily expressed in myeloid cells are among the most distinct, all of them in these red top-heavy hourglasses. They are overexpressed in patients that are non-responders to checkpoint inhibitors. In this case, this is data from relapsed refractory melanoma patients. Our programs are focused on blocking these four receptors to flip these macrophages from sending signals that suppress immune attack to sending signals that encourage immune response to it, effectively reprogramming them to help rather than hinder detection of the tumor. Here are how our drug team has mapped these promising myeloid cell targets. NGM707 blocks two receptors, ILT2 and ILT4. It is the only dual antagonist of these receptors in the clinic, and I'll explain in a moment why we think this is a superior strategy. NGM831 and NGM438 are both designed to overcome a particular form of tumor resistance called the myeloid stromal checkpoint. NGM831 is an antagonist of the ILT3 receptor, and NGM438 is an antagonist of a receptor called LAIR1, each of which I'll describe in a little more detail shortly. Let's take a closer look at each of these programs, starting with NGM707. We are the only company developing a dual inhibitor of ILT2 and ILT4. This approach has some important benefits. First, ILT2 and ILT4 are closely related receptors with high homology and overlapping expression patterns. Both function as receptors that, when activated, promote an immunosuppressive phenotype. In this image to the right, this is an analysis of receptor expression in immune cells associated with a patient's tumor biopsy. The yellow dots represent myeloid cells expressing both the ILT2 and ILT4 receptors, suggesting a high degree of redundant expression and perhaps redundant activity. Separately, ILT2, the red dots, show up in key areas on the plot, though, namely B cells, NK cells, and certain T cell populations. This suggests a potential inhibitory role for ILT2 in certain T cell populations as well. This expression data together with functional data and these two receptors appear to be partners in crimes that restrict antitumor immunity and promote a tolerance to the tumor that contributes to T cell checkpoint inhibitor resistance. NGM707 entered the clinic in the middle of last year, and we are advancing through the single agent dose escalation portion in patients with advanced solid tumors. We expect to advance to a dose escalation phase in combination with an anti-PD-1, specifically KEYTRUDA, shortly. We think that by blocking both receptors, we can overcome redundancy of activity of the two receptors. In other words, targeting only ILT4 or ILT2 may not fully release this myeloid cell checkpoint, making our dual antagonist approach a more complete blocker of the biology and a more potent partner with an anti-PD-1. We're very excited about the potential of this program from both our own preclinical data and also from initial clinical data from an anti-ILT4 only inhibitor. I'll cover some of the preclinical data in a moment. Merck shared some initial clinical data from their anti-ILT4 antibody several months ago, showing even just inhibiting ILT4 drove a gained response in combination with KEYTRUDA in patients that had previously progressed on KEYTRUDA alone. We view this as very promising and perhaps a minimum of what we'll see with our dual antagonist approach in NGM707. Let's now take a look at one of several pieces of preclinical evidence we have that supports the rationale for this approach. This is a study done in human immune cells in vitro looking at Fc receptor signaling on myeloid cells. The key takeaway is here on the right looking at how blocking ILT2 and ILT4 drives significantly more activating cytokine release. You can see the green curve going up when we've blocked both ILT2 and ILT4, compared to blocking either ILT2 or ILT4 alone in the blue and red lines. So additive, if not synergistic effect in blocking both receptors over either alone. We'll now turn to our anti-ILT3 program called NGM831, which is entering the clinic this quarter. ILT3 is also an immune inhibitory receptor that is highly expressed in tumor-associated myeloid cells. We identified and published the finding last year that one of its key activating ligands is fibronectin, which in turn is a major component of the matrix or stroma that solid tumors are partially composed of. This was an important insight to connect some dots in tumor resistance because it's known that high ILT3 expression in several cancer types is associated with poor survival, and similarly, fibronectin is upregulated in several cancers and associated with tumor progression. Both appear to be bad guys, in other words, in the context of anti-tumor immunity. Our approach with NGM831 was to make a high affinity antibody to block the activation of ILT3, including its interaction with fibronectin, highlighting how our capabilities in receptor ligand de-orphanization and our discovery engine can translate to differentiated product candidates. Our hope is effectively to flip the switch on tumor-associated myeloid cells to drive more activating cytokine release to encourage rather than discourage T cell infiltration and attack of the tumor. We think this approach could be particularly powerful in combination with an anti-PD-1, and we'll be sharing additional preclinical work through the course of the year to support this idea. Now let's take a look at the third program in the myeloid checkpoint portfolio. Our interest in LAIR1 is parallel to the ILT3 story I just told you. LAIR1 is an immunosuppressive receptor and binds and is activated by collagen, the other major component of tumor stroma in addition to fibronectin. Both LAIR1 and collagen are upregulated in certain cancer types and drive immune suppression in the local tumor environment. A similar idea to the ILT3 fibronectin partnership. NGM438 is a first-in-class high-affinity antibody we have designed to block LAIR1 activity, and we expect to dose our first patient in the second quarter. We believe that by blocking LAIR1, we can reverse immune resistance, particularly in high collagen-expressing tumors. Here too, we seek to potentially broaden and deepen tumor responses to T cell checkpoint inhibitors like anti-PD-1s by addressing both the T cell and myeloid cell checkpoints that tumors use to evade immune response. We have a variety of preclinical studies that support the activity and rationale of the program and plan to share this data in 2022 in addition to the first patient dosing milestone we expect in the second quarter. To pull it all together, I wanna remind you that by the middle of this year, we expect to have a total of seven programs in the clinic, and all of them come from our in-house discovery engine. They're built on the foundation of important biological discoveries made by the team at NGM through exploration of novel disease biology, and they are proof of the utility and repeatability of our approach. Product testing tends to exceed what we can develop in-house, and we expect to continue to leverage partners for capabilities and funding, particularly in our non-oncology research areas. One number on the lower right of this slide speaks volumes about our business model. About 50% of our funding to date has come from these business development activities. Touching on our financial profile, we ended the third quarter with $383 million of cash and guided that our cash runway should take us to the first half of 2024. I'll emphasize the point I was making a moment ago by pointing to our related party revenue line, which stems from our Merck relationship. It's a good reminder that business development revenue has been a key part of our business model to date. What this strong financial profile enables us to do is execute across our pipeline and continue to generate a diverse set of catalysts that drive value rather than have to put all of our eggs in one basket. You may not be surprised to hear that companies like Seagen and Regeneron inspire us, and our intention is to follow a similar blueprint in building our company for the long haul. Looking at the quantity and variety of programs we have in development and the milestones we are looking forward to in 2022, I feel we're well on our way to this ambition. Using the foundation of our powerful discovery engine and selectively entering partnerships to enhance our late-stage development capabilities will ultimately propel us to become a self-sustaining biologics powerhouse with multiple approved products and a renewable resource of lead candidates from the discovery engine. Thank you all for listening, and I will now invite our CFO, Siobhan Nolan, and Judy to join me on the screen here, and we would be happy to take any questions. Thank you very much for that, David. Just a reminder to the audience that if you'd like to ask a question, please submit it through the blue box at the bottom of your web page. With that, I've got the first question that's come through is, what do you see as the most significant value creating catalyst across the next 12-18 months at NGM? Yeah. We've got, obviously, as I just said, coming this, our NGM621 CATALINA trial in the fourth quarter. I think that'll be quite validating or revalidating of the mechanism, our approach in particular with our monoclonal antibodies blocking C3. But then separate from that, we really have quite a bit of data to come across our oncology portfolio. As you know, in oncology, the data from these clinical trials is less punctuated in moments in time. We'll be sharing data from our NGM707 program, the dual ILT2/ILT4 inhibitor, towards the second half of the year from our phase Ia portion. We'll have additional data from our NGM120 program. One way to think about it is you should expect some of the regular attendees at oncology medical meetings going forward with a collection of data that we think will support this myeloid reprogramming hypothesis generally. Even further out, looking into the first half of next year, we do expect to have our ALPINE 4 data with aldafermin in the cirrhotic NASH population. We think that would be really interesting because while we've seen quite a bit of activity from that drug over time in the NASH population, this will be the first time we're studying the drug for a full- year of treatment, and that's obviously a very advanced patient population with great need. Got it. Thanks for that, David. How do you see the marketplace for GA therapeutics unfolding in the coming years, considering there are no approved therapies today, but obviously several late-stage developments, including NGM621? Yeah, it's a really obviously big opportunity. Over a million patients in The U.S. alone, 5 million worldwide. Likely these patients have a variety of ways they end up getting to the GA state. That's usually an equation that when you fast-forward how the marketplace develops, requires multiple tools in physicians' hands to combat the disease. If we look at what we think is very analogous in the wet AMD market, you can see that the initial programs that are approved or the candidates that are approved are hugely important, and they can validate a mechanism. Particularly in the retinopathy space, it seems that relatively small differences in programs. It can even be the format of these deliveries from the time sensitivity in a doctor's office delivery. They drive relatively large changes in market share. I think there's likely a future where there are multiple programs that have some portion of the market that will probably, importantly for patients' benefit, drive towards the most convenient, safe, and efficacious drugs to treat the disease. Got it. Thanks for that, David. How does NGM intend to commercialize the NASH asset in The U.S. and the EU? Yeah. Well, we have two NASH assets we consider. There's aldafermin, which is wholly owned by NGM, and then Merck has already licensed NGM3655. We used to call it NGM313. They're running a global phase IIb trial in non-cirrhotic NASH. To answer your question, NGM3655 already has a partner for late-phase development in the form of Merck, which we're thrilled with. Separately on aldafermin, what we plan to do over time is likely find a partner for that program for both the U.S. and Europe. Fortunately, we don't have any immediate urgency for that. We frankly plan to read out ALPINE 4, really have a what we hope to be a robust data set for the activity of the program overall and then continue partner conversations at that time. Understood. What are the different partnering scenarios with NGM621 post-CATALINA? We understand if Merck exercises their option, NGM can obviously opt in via the royalties or milestones or also have the option for, you know, co-prom profit share. What do you think about these options? Siobhan, would you like to cover that one? Sure. I'm happy to start. As you alluded to, this program falls under a long-standing collaboration we've had with Merck. David mentioned they optioned NGM3655 for F2/F3 NASH patients. This is also optionable after the CATALINA readout. At that moment, Merck will have the ability to option NGM621 as well as a couple undisclosed retinal targets, so there could be an ophthalmology bundle that Merck takes forward. Maybe just a little additional color. We are working very closely together right now in GMP manufacturing, as we think about potentially having that conversation. As you alluded to, if Merck makes their decision to proceed forward, NGM has an option of whether to participate in the up to 50/50 gross profit split, which we're very interested in and inclined to due to the market dynamics that David talked about. If Merck does not option the program, then NGM has a wholly owned program with worldwide rights. Given our conviction about the market opportunity, we'd be very excited about that option and talking in terms of partnerships with other folks. But at this moment, we're proceeding forward with wrapping up CATALINA in the fourth quarter, and the decision for the option will be in the following quarter. Got it. Thanks for the insight there, Siobhan. NGM 707 is obviously generating a lot of interest as a next generation IO candidate. I think some investors question why Merck would have left this outside of the scope of their renegotiated collaboration. Is there any particular data they saw in that? We actually view it as an opportunity. I think it's pretty well observed at this point. There's There's pressure at Merck to diversify away from oncology. When you're a company as big as Merck, that scope is pretty large. Historically how we've been working with Merck is they actually use this as a sensor to go into new areas. NASH is a good example. You know, since they've licensed MK-3655, they've actually built assets around it from other sources. Similarly, moving into the back of the eye with a retinal drug like NGM621 would be a relatively new move. We like to use this as a tool for diversification. Actually, we happen to overlap on targets in immuno-oncology because promising for the potential of those targets and two relatively smart companies ending up in the same place. But it was a little bit too much concentration in the portfolio, so no desire to grow that. I think it's also important to remember too that Merck still owns 17% of NGM. While they gave up a specific option on the program, we still have a very close relationship with them. If you know, we were to produce data that knocks the socks off of them and others, they're not out of the game, so to speak, to having access to the program. We certainly have a lot of conviction in this dual inhibitory approach. We're really eager to see what clinical data contributes from the program. Got it. Makes a lot of sense. Thanks, David. What should we expect coming out of your discovery engine next? Yeah, it's a bit of a secret there, David. Yeah, it's constantly moving away. We have about 100 scientists at NGM that are working on that kind of next frontier in biology. It's, you know, I've been with the company for six years, and it's often hard to predict which one of those will actually be the next candidate. It's a pretty brutal process. It's not like we have one candidate moving forward. There's a competition internally to what is that best candidate to earn that next slot. One of the new features we have now, though, after our renegotiated Merck partnership, we actually are sort of back in the market from a business development point of view. As evident from our broad pipeline, we're being really careful about not overloading it from both a financial resources but also from a human resources point of view. That, you know, we're trying to keep a relatively lean team helping into these programs. Now we have this new avenue that we can work with the discovery engine in terms of maybe we don't have to take it all the way to clinic before we partner. That's keeping Siobhan really busy in her team, as she leads business development. I can't give you specifics at this point, David, but just rest assured there are things under the waterline, so to speak, at NGM that will be coming forward. Got it. Thanks for sharing as much as you can, David. Look forward to seeing what's next. I think you touched upon this just then and also throughout your presentation. David, Siobhan, given you now have a portfolio of, you know, quite a few wholly owned programs, what are you guys looking to do with these in terms of partnerships? And are you guys looking more into that? Yeah. Siobhan's gonna answer that one. Sure. You're right. We're thrilled that we have a portfolio of wholly owned oncology programs, as well as everything that's coming out of the discovery engine that David was talking about. We have a lot of conviction about the programs, and we're moving as urgently as possible with these programs in the clinic. That being said, I think we also recognize that, you know, as we get into later stage development, there's some piece to be had from pharma partners and oncology leaders. We wanna be, you know, thoughtful about how to do that and really amplify the programs that we have. We're in a very fortunate position that given the balance sheet that we have, $383 million at the end of the third quarter, we can be very flexible and be really thoughtful around what we want to do. You know, we started to do things. We did a PD-1 supply agreement with NGM707 at the end of last year. It's non-exclusive, but it's helping us, again, be interested in how we wanna be partnering in the future with these programs. Got it. Thanks for that, Siobhan. I think we're getting pretty close to time. With that, is there any closing remarks, anything you'd like to leave with the audience? Sure, yeah. I think 2022, as I started with, is setting up to be a really exciting year at NGM. You know, one of the things we like to hear when we're speaking to the investment community is it's not uncommon that they focus on one particular asset in NGM, but part of the conversation, there's sort of this, "Oh, I didn't know you had a complement C3 inhibitor or a dual blocker of ILT2, ILT4." I would say encourage everybody to make sure you're looking for the whole elephant, so to speak, of NGM, because we have a lot of exciting assets, and it's a little different given the breadth and in terms of what we cover. There's a lot to dig into, and we're always happy to do that. I think we'll have a lot of validating data through the course of 2022 to really even build that out further. Oh, well, Siobhan, David, it's been an absolute pleasure, talking with you guys. Thank you very much for your time and presenting at this year's conference. Thank you, David. Thanks for having us. Thanks, guys.