WCLC 2026 Highlights: Evolving Strategies in Late-Stage EGFR+ NSCLC

In this expert panel, faculty examine emerging World Conference on Lung Cancer 2026 data in epidermal growth factor receptor-positive (EGFR+) non-small cell lung cancer across late-stage disease. The discussion explores the long-term safety of combination therapy, the role of TP53 and other co-mutations in prognosis and treatment selection, and how EGFR+ subtype may influence first-line strategy.

To hear the early-stage panel discussion, click here.

Transcript

Eric Singhi, MD: All right, so there's a few studies that we'll highlight in this space. The first one is long-term safety outcomes with osimertinib plus platinum-pemetrexed in EGFR-mutated advanced non-small cell lung cancer. So this is the FLAURA2 phase 3 trial. Obviously we know that we got both PFS and OS benefit in the frontline setting with this combination of osimertinib plus chemotherapy strategy, but this is a really nice post hoc analysis that's showing us, from a longitudinal perspective, what's going on with the safety of the FLAURA2 regimen. 

I love studies like this because I'm a big believer in counseling our patients. They don't want to know what's going to happen that same day, that next week, next month, but even along the whole treatment journey, what can they expect in terms of safety? What can they expect in terms of efficacy outcomes? 

We've had updates very nicely about the efficacy about the PFS and the OS, but what's going on from the safety perspective? 

Really the key results that we're seeing, and I think the main takeaway from this is that the toxicity profile with FLAURA2 is not static. It's actually dynamic, and it's dynamic in a favorable way. 

And so, what you can see is that at induction we have osimertinib plus both platinum and pemetrexed. So we've got the 3 drugs, but then at maintenance we drop, obviously, the platinum, we go to osimertinib and pemetrexed. And then there is an opportunity for a chemotherapy-free regimen with just osimertinib alone. 

And you can see, as patients make at each milestone kind of every touchpoint throughout this journey, the treatment related grade 3 adverse events, new treatment related grade 3 adverse events continues to decline. So, 43%, 25%, 14%. 

Now there is some bias here, right? We have patients that are longer-term survivors as they make it through this journey. There's treatment-selection bias as well, but I really like highlighting this fact that the toxicity profile is more dynamic as opposed to static, and that there is an opportunity for patients to kind of approach that chemotherapy-free regimen. 

The types of toxicities that you see, so obviously in the beginning with induction, you're going to have more of a cluster of hematologic toxicities. And then, when you get into the maintenance with osimertinib-pemetrexed, you really need to be watching for renal adverse events. So anemia, fatigue, the elevated serum creatinine are the ones that I'm really looking out for my patients that are on pemetrexed maintenance. You do not want to burn the renal function, because we want to continue to preserve that for clinical trials. And so, I think that's really, really important to keep watching, especially for fellows, keep an eye on the serum creatinine over time. So really nice counseling strategy for patients based on this data. 

The next study here, so we're continuing with this TP53 theme. So this is looking at baseline co-mutations and acquired resistance mechanisms in patients that have EGFR-mutated advanced non-small cell lung cancer, again, an exploratory analysis from FLAURA2. 

And so, what you can see here is that almost two-thirds of patients actually had a co-mutation in TP53. So it's pretty prevalent. There's no surprise to this. It's a very common co-mutation that can coexist with EGFR mutations. And what they wanted to look and see was, based on these co-mutations at baseline, what's going on in terms of acquired resistance patterns, how are patients doing in terms of progression-free survival? 

My key takeaways from this is that I am not going to use, I'm going to be asking the panel this as well, but I'm not going to be using TP53 wild type or mutant status to make my decision in terms of, do I add in chemo or do I not? I don't think that that's the right thing to do for patients. One, because you can see that, regardless of the TP53 wild type or alteration status, really the combination therapy is favored for both. And so, I think that's not the only determinant here to make in terms of status. 

I do think it's interesting, when they looked at the acquired mechanisms of resistance for these patients, quantitatively that landscape was different. And so EGFR C797S and RB1 mutations were less commonly seen if you added in chemotherapy to osimertinib as opposed to osimertinib alone. So I think that's really a hypothesis generating that may explain some differences in terms of the biology and this does warrant some prospective study, but overall pretty interesting to see, but not really practice-changing for me. 

And then, last but not least is updates from the PALOMA-2 study. So, PALOMA-2, as a reminder, was looking at first-line subcutaneous amivantamab plus lazertinib, another combination strategy and important combination strategy for patients with newly diagnosed EGFR-positive non-small cell lung cancer. We already knew from PALOMA-2 that subcutaneous amivantamab plus lazertinib had a nice response, had a nice safety profile, and it was also consistent overall with the historical IV data that we had with IV amivantamab. 

And so, this was looking at longer-term efficacy and safety for these patients. How did they do? Again, this was a phase 2 study. Patients were treatment naive. They had one of the canonical EGFR mutations, as you can see, just over 200 patients. Subcutaneous amivantamab, of course, was given with this loading dosing weekly for the first 4 weeks, and then they were able to transition to every 2 or every 4 weeks. Lazertinib was given once a day. 

The key takeaway here was median PFS was 26.1 months. Remember this was a single-arm study, guys, you can't really make those comparisons in terms of how things went on MARIPOSA for example, but just something to keep in mind in terms of framing that timeframe of 26.1 months. And then, you can see median OS was not reached. The administrative-related reactions, ARRs, that's what that stands for, occurred in 16% of patients, but thankfully grade 3 or higher was 0.5%, less than 1%. So that was really reassuring. 

So, I think really what this is telling us is not so much the efficacy story, but the administration story of amivantamab. And I hope, I pray that if you're giving amivantamab in your clinic, you are no longer giving IV amivantamab, it's done. We really need to be giving subcutaneous amivantamab for these patients for these reasons. One, we're seeing good efficacy, and second, we have a significant reduction in adverse-related events, such as administrative-related reactions. 

I do want to tell you though that subcutaneous amivantamab does not solve everything in terms of the toxicity profile. So please, the COCOON regimen is really important in terms of the dermatologic strategy. You need to be giving anticoagulation to your patients as well, particularly during the first 4 months. Sometimes you need to prolong that based on different risk factors of patients, but it's really reassuring to see that the efficacy is there, and that we saw an improvement in safety for our patients in how we deliver this very important regimen. All right, thank you. 

Sarah Goldberg, MD—Moderator: Great. So we've had these regimens now, FLAURA2, MARIPOSA, for a couple years. More and more as we get more data, especially the OS data, I think many of us have been convinced that we should be defaulting to combination. This is always the question that nobody really knows the answer to, I'm pretty sure. How are you thinking about selecting? So, are you doing what I'm saying, defaulting to combination, but saving single-agent for select patients? And then, what about the different regimens? Are you talking to patients and giving them the menu or really selecting based on characteristics? 

So Eric, do you want to go first after your great presentation on the different regimens? 

Sr. Singhi: And you guys will come to the debate and you'll get the answer with Dr Yu after lunch. 

Dr Goldberg: Sorry. 

Dr Singhi: No, you're good. You're good. 

Dr Goldberg: Which side are you debating? I couldn't tell. 

Dr Singhi: Combination. 

Dr Goldberg: Okay. 

Dr Singhi: Yes. And that is my default. I'm going to tell you that is my default for probably 90 plus percent of my patients. At MD Anderson, I'm the leader of our young-onset lung cancer program, so the majority of my patients are under the age of 50. These are patients that are super fit, patients that you never would've though would've gotten lung cancer, and there they are, presenting newly diagnosed. 

And so, many of them want to be aggressive and many of them are able to be aggressive, and we talk about combination therapy. When I'm thinking through this, it's really important to me that I counsel patients on all 3 options because if you don't talk to them about all 3 options, they have either already gone online and read about it, or they're going to lose trust in you because they're going to go online afterwards. They're going to find the EGFR groups, and they're going to hear people's stories about being on different regimens. And then they're going to message you, call you and say, "Why didn't you tell me about all 3? I heard about this option. Why didn't you talk to me about it?" 

So, I actually talk to my patients about 4 options. The fourth option is clinical trials, and I think that's really important. We shouldn't reserve clinical trials until a last resort. There's also very good clinical trials that are actively enrolling in a frontline setting. 

When I'm thinking through how I counsel patients, I use exactly this terminology here with the 3 buckets. So, I'm thinking about disease characteristics, molecular characteristics, and then patient characteristics, particularly the patient right in front of me. So disease characteristics, I'm thinking about where is the disease located? How heavy is the disease burden? Is there CNS disease? Those are really important factors to me. 

Molecular, we're not just saying EGFR positive, we're truly thinking about the subtype mutation. We're thinking about co-mutations, we're thinking about other alterations that might be involved. 

And then, the patient characteristic is arguably the most important. How aggressive do they want to be about their treatment? Are they able to commit as much time to coming to the infusion center to... Now we're not getting infusions as much if we're not doing a chemo regimen, but are they able to come to truly match the therapy, the time course that's required? And then, what do they want out of their treatment? What side effects are they okay or not okay with? You have to ask patients about this and this takes a lot of time. 

So my patients, usually it's almost 1 to 3... It's never 1 visit where they make the decision. It's usually over the course of 3 visits and talking to 3 different providers, myself, my APP, and my pharmacist. And so, it takes a lot. These are the visits where my nurse is knocking on the door saying, Dr Singhi, get out of the room. You've been in there for 90 minutes. So, it's tough. 

Dr Goldberg: Yes. It's good to have options, but it does make it more challenging to have these conversations and to select. 

Eddie, I'll ask you, we hear a lot about these high-risk features. TB53, we just saw some data on, clearly a high-risk feature, brain metastases, liver metastases, ctDNA positivity. It's pretty consistent across studies. Are you using those to select combination versus not, or even the different regimens? Is there any feature like that that we can use? 

Edward Garon, MD: Sure. I absolutely am not using them to select for patients. And, I think that when this data originally came out, what we hoped as a community would happen was probably illogical and didn't. What we would've liked to see is that the benefit is disproportionately in patients who have poor prognostic features, because then we could tell them, "Well, we need to escalate in your case and it's worth it." And then, the rest of the people we would say, "Oh, you can just get the better-tolerated regimen." But in fact, the relative benefit appears to be similar across the board, and simply people with poor prognostic features are going to do less well, but derive proportionately the same amount of benefit. 

So, I really only use patient goals. And when you discuss it with patients, I actually find that it breaks down pretty clearly. There are some people who are very reluctant for the idea of chemo and we say, "Okay, well, it is an option to take single agent." And then, a lot of people who, be like, "I have metastatic cancer, why would I take any sort of step down in therapy?" 

And so, I found my patients to be pretty self-selective in this. The only conceptual problem I have with it a little bit is, I still worry that some of the survival data is based in a global study on access to subsequent therapies. So, in my own mind, I think that the stated survival benefit is probably stronger than what we would experience in the United States, at least. And so, that's why although most of my patients do end up on an intensified regimen, there's a substantial percentage that do opt for osimertinib monotherapy and is definitely not a situation where I aggressively try and bully them out of that if that's where they are. 

Dr Goldberg: I like the way you say, self-selected. I've found that too. I mean, the conversations are not short, but I don't know that I've found them to be so challenging in some ways. I think a lot of people, when you say you could get a bad rash, they're like, "No, I'm working. I don't want to tell people." 

So, I think a lot of people, it's very clear. There's the, "I never want chemo ever, people, and then there's the, "I never want a rash," people." So I think sometimes it's a little easier than 3 visits. 

Jamie, I wanted to ask you about brain metastases. That's so common. Are you picking a regimen based on that in terms of, I think usually as well talked about, combinations are typically what we're thinking about for these patients. Do you have a favorite for patients with brain mets? Are you thinking about radiation upfront? How are you thinking about that? 

Jamie Chaft, MD: The presence of brain mets makes me lean more towards a combination, and encourage the patient to be more willing to accept a combination. I use radiotherapy as consolidation for suboptimally responding lesions or critical lesions, but I don't, I almost never recommend upfront radiotherapy unless it's a critical lesion. 

In terms of choice of regimen, the characteristics of the brain mets have a big component. If they're hemorrhagic, that will push me away from the combination ami-laz [amivantamab-lazertinib] because of the requirement for the DOAC [direct-acting oral anticoagulants]. But then you also have that same concern about thrombocytopenia on chemotherapy. So, it leads to more of a sequenced approach of starting the OSI, getting control, and then adding the chemo. 

Dr Goldberg: I just wanted to ask, you talked about toxicity with ami-laz and the improvement in terms of infusion reactions. There still are reactions to the subcutaneous but significantly lower, not really, very few high grade. How are you finding the regimen with the subcutaneous form, with the prophylaxis? A lot of our nurses, especially whenever I want to start ami-laz, they're like, "Ah." They're very anxious because they're thinking about the prior generation of when we're using IV, and didn't have as much prophylaxis, but we still see toxicity. 

So, are you finding that it's much more tolerable? Are you still seeing challenges? Do you have any way of how do you counsel patients on what to expect, I guess, Eric? 

Dr Singhi: Yeah, so I think the counseling aspect is huge. It's really important. You have to stress these patients, this isn't a reactive strategy, this is a proactive strategy. So, I actually make them take pictures of how they have their whole skin set up and make sure that they have their anticoagulation and everything is ready. Thankfully, we have all that built into our order set whenever we're ordering amivantamab. 

The other thing that I also do whenever I'm prescribing amivantamab is they get a dermatology consult. So, it takes time to get into dermatology, even if you don't have a cancer problem. It took me almost 12 weeks to get into a dermatologist, but that's immediately something I'm doing because the rash is tough if it does happen. We do have really good COCOON regimens and strategies that are meant to be preventative, but how do you react when patients still have rashes? I think that's difficult. 

Dr Goldberg: It's like COCOON-2. 

Dr Singhi: Right. 

Dr Goldberg: Elastic dermatologist. 

Dr Singhi: Yep. Yeah, exactly. 

Dr Goldberg: I like it. Okay. Any other comments from the panel or shall we move on? All right, move on. Eddie, you're up. 

Dr Garon: Thank you. So, this is an interesting analysis because it addresses a very significant real-world problem. I remember one patient in particular, Jonathan Goldman and I have worked together for over 15 years at this point, and it was a patient on a study of his, but it was a patient of mine and he needed to see them for some visit. And they had a fairly large brain metastasis. 

And it was interesting because to one of us, it was very clear that we should radiate this first, and the other was very clear that we should just wait for the targeted therapy. And we both recognize, as you can imagine, over that time, our treatment generally converges, but we both realize there's no great data for this, and there's still no great data, but this is a combination of 2 randomized studies that were conducted that were looking at patients. 

They had to have no more than 10 brain metastases, and the largest could not be more than 3 centimeters, and they had to either be asymptomatic or not, or mildly, at most, symptomatic. And patients were randomized to get SRS [sterotactic radiosurgery] and then osimertinib, or just the systemic therapy alone. 

Again, it's 2 separate trials that were basically merged for analysis, and the results are actually a little bit surprising and not supportive of the stereotactic radiosurgery. When I talked with trainees about this and we talked about, for instance, prophylactic brain irradiation for small cell lung cancer, I always explain, if you prophylactically irradiated people's right arm, they'd have less mets to their right arm too. But the question is, are you going to increase the overall good outcome from that patient? 

The interesting thing is, here is, the equivalent is the right arm got more metastases, or at least didn't do any better. So if you look here, the response rate actually was higher in the osimertinib group than it was in the osimertinib and stereotactic radiosurgery group. And you can see the waterfall plot there, showing that actually the depth of response and the frequency of response looked better. 

Now, one potential explanation is that these results are confounded by the effects of radiation, that somehow inflammation related to the radiation made it so that you didn't see a response, but nonetheless, makes it a little bit hard to be really enthusiastic about upfront radiation, at least in meeting these patients. 

Now, how do you do that exactly when you have a study of 80 patients? A little hard to know. For instance, the patient that I'm talking about that we had a disagreement, they were right near the edge. It was a single lesion right near the edge of that size cutoff. So, does that mean that that person should go one direction or another? It's a little hard to know from a small study, but at least this would support that maybe it's not that important to get radiation upfront when you have good drugs that you anticipate being effective. 

This is a, looking at sort of, you have this data, but there also was sort of a real-world data looking at consolidative ablation in patients after they've received treatment, to then treat their brain metastasis. This, I would say, has become almost a polarizing idea across the community. Oftentimes, radiation oncologists, they really like this idea of, you've treated the disease, it's gotten to its nadir, and now you zap what's left and everything gets better. There are some theoretical reasons to imagine it being a good outcome. There also are some small randomized studies that have been supportive. The large randomized study was not supportive of the idea. 

This is a real-world analysis, and at least I would say leaves this question open and I think will continue to be, I'd like to say discussion, but it may sometimes be closer to argument between the medical oncologist and the radiation oncologist. I'm seeing some nodding. I may be not the only one who ever has to engage in this argument. 

So, this is another interesting day. This is a novel, some people are calling it a fourth-generation EGFR inhibitor. I always caution people that there's no exact definition of what a generation is, and at least prospectively. So, it's a little bit hard to know what to make of this. But one of the things they're looking at are patients with secondary resistance mutations, and this was patients with C797S mutations. There was a whole class of drugs that inhibited, that basically treated both C797S and T790M. 

And, the importance of that is a little bit unclear, because that tended to be a bigger problem when we started patients with erlotinib for instance, and then moved to osimertinib. But nonetheless, here you see that in this population that nearly half of the patients had an objective response. And, I would argue the duration of response data is maybe good, not great, from this. 

One of the questions is we already do have EGFR inhibitors, earlier-generation EGFR inhibitors are effective in this. And so is this adding on that? I would say that this is a small study and it's still a little hard to know. You can see they say in their conclusions that this is true for afatinib-treated patients as well, but when I at least eyeball the chart, it looks like they had 7 afatinib treated patients, but only 2 of those were responders. If you can look through the gray for the afatinib. And so, I think that this is a drug that people are excited about. This at least gives some proof and concept and we'll see how it evolves over time. 

And then, I think this is the last slide that I have, which is really sort of a whirlwind through 3 separate trials, and we can discuss it in the group. The PAPILLON trial was a study in patients upfront EGFR exon 20 insertion. This study did not have a survival benefit, but I think that's a little hard in that it was surprising to me because we actually had this study and had trouble rolling people over, based on the requirements. But over 3 quarters of the patients did cross over to amivantamab. And so, the survival data was negative, but it's unclear whether that is just based on getting later amivantamab. 

REZILIENT3 showed that progression-free survival, when you added the EGFR TKI in exon-20 patients, was longer than chemotherapy alone, did come at a substantially increased rate of high-grade toxicities. This was mostly hematologic toxicities, but at least the raw number is very significant, but also a positive study, clearly, for progression-free survival. 

And then, the last one is a smaller study, phase 2 study, which sort of is another study in this sort of field of adding anti-angiogenic agents to EGFR inhibitors. And this study is relatively small, but I would say is generally consistent with what we have seen across the field, which is a clear benefit in progression-free survival. But, we're at an early time point in this. Historically, most of these have not translated to an overall survival benefit, but this is early on this study and a small study to boot. So we can go have the discussion. 

Dr Goldberg: Thank you so much. So, let's talk about local therapy first. And we heard a question about this before, and it was nice to see the data, so now we can speak to it. 

Jamie, you mentioned that you're not really giving radiation upfront to these patients. But Eddie, I totally agree there's a lot of debate. What do we do after we start treatment if we still see the disease? Obviously, if someone has a complete response, fine, but if you still see the disease... 

I will say I have a debate tomorrow here on this topic, very nervous, but it really is an outstanding question. But I always think when you don't really know the right thing, where we have some data that supports it, some data against it, it's all phase 2, what do we actually do in practice? 

So Eric, do you want to tell us your thoughts? Are you giving local consolidation therapy if someone does not have a complete response, and maybe separating brain versus- 

Dr Singhi: That's what I was going to ask. Yeah. Are we talking brain? Are we talking outside of the brain? 

Dr Goldberg: Well, maybe both. Tell us both, or pick one and answer that. 

Dr Singhi: I'll pick the one that I get, the consult that I get all the time. So my institution is very pro LCT [local consolidative therapy], so I get patients, multiple patients every single week that travel from around the country to come see our teams to ask, "Can we do something more than systemic therapy alone?" 

And that used to be a question that was ridiculed for patients with Stage IV disease, but now I think it's a very valid question as our treatments get better, as we get smarter at really targeting the biology. And we have data now that is coming out that is showing for patients with EGFR disease that it is a very valid strategy to consider. 

So the data I'm referring to is actually from the NorthStar trial that wasn't shown here, but I think it's very valid. It's phase 2 study where patients received osimertinib. And what we saw was that for patients that got induction systemic therapy and they were randomized to either get systemic therapy alone and continue with that, or systemic therapy plus LCT, there was an improvement in progression-free survival for patients that didn't receive LCT. 

A lot of you may say progression-free survival, is that really meaningful? We don't have the OS data yet. For a lot of these patients, being able to continue on an oral therapy, one that's arguably very well tolerated for a longer period of time, is also a meaningful outcome for these patients. Osimertinib really becomes like their blanket, their safety blanket, if you will, on this disease, especially if they're tolerating it well. And so, if I can buy my patients more time on the therapy that they tolerate better, I think it's really important. 

I will say that LCT is not the right answer for everyone. So I have a rule of 3. We've written about this rule of 3 for patients when we're considering LCT. It's got to be the right patient at the right time with the right team. So, it's got to be a patient that is fit, that believes in wanting to augment their therapy if that's a possibility. It's got to be the right time, and that's still debatable. So for NorthStar, it was 6 to 12 weeks on induction therapy before they were considered for LCT. Is that enough time? When is there a time point where it's sailed and maybe we shouldn't be considering it? I think that's important. 

And then, last but not least is the right team. So we're really, really stressing this message that they need to be seeing surgeons that are experienced if we're going to consider surgery for consolidation. They need to be seeing radiation oncologists that know how to manage potential toxicities that may develop, like pneumonitis. So that rule of 3 is really important. 

Dr Goldberg: We are a little low on time and I want to answer these next 2 questions, because they're really important too. So Eddie, I'll ask you the second one. You showed us the data for a novel EGFR inhibitor for C797. Are you always testing for these alterations at progression on an EGFR TKI? And then, which ones are you acting on standard... I won't say standard, but which ones are you acting on if you don't have a trial? I'm sure we all like to enroll patients on trials when we have that option of a targeted therapy on a trial, but which ones would you consider off of a trial? 

Dr Garon: So, this is something I actually feel strongly about. So, we end up getting a lot of these results, maybe not on everyone, but a lot of them, but a lot of it is in all honesty for clinical trials. I worry that, in general, we do more harm than good with these outcomes, and that we're trying to turn every oncologist everywhere into, that they're going to develop their own home brew when they get the results back from the NGS test. "Oh, I think this person needs a splash of cabmatinib. This one maybe would benefit from this." And in the end, we're asking people to do things that are totally unfair. So, cabmatinib is a great example. What's the right cutoff for what's amplified? Who knows? Should you give full dose cabmatinib? Seems like a lot. 

But are these good answers? This is not what... To me, this is not what we're supposed to be doing as academics. And this is what you always try and explain to people that they don't. They're not coming to see me because I'm more clever than the person who sent them, and that I'm going to be able to devise a little of this and a little of that that nobody else could. And so, I think it's a little bit cautious. 

So there are times where we've looked at, at is, I think that it becomes hard to ignore when you see a very clear driver. We've seen things like ALK gene rearrangements, BRAF V600E, but we definitely have seen patients who respond to these, but we also have definitely seen toxicities, as would be expected when you start combining drugs that don't have large data sets supporting them. 

So, I think that I would continue to encourage people, first look for a trial, and although you can do it, recognize the limitations that you generally don't know the efficacy in a robust way, and you also don't have a great sense of what the toxicity is. 

Dr Goldberg: Okay. So let's try to touch on this last question really briefly because we're out of time. But these uncommon mutations, we used to not have too much data. Now we actually have some data. So Eric, how are you thinking about treating first line, your exon 20s and your atypicals, in 10 seconds or less now? [inaudible 00:29:17] 

Dr Singhi: Yeah. Well, I'm looking at my continuity clinic fellow, because we just had a new patient, young patient that came to our clinic Thursday afternoon with an atypical compound EGFR mutation, and I really appreciate the data that continues to evolve. I think it's a huge area of unmet need. So there is the ALPACCA study that's actively enrolling right now, so that's one to consider, and that's a trial that we presented to our patient, and that's the priority. 

But otherwise, the data from amivantamab plus lazertinib for these atypical mutations from ASCO has really solidified my practice compared to historical outcomes with apatinib. I really think that that is not my preferred choice anymore, is amivantamab plus lazertinib. 

Dr Goldberg: I agree. Remind us what that trial is. What the ALPACCA trial? 

Dr Singhi: ALPACCA trial is looking at firmonertinib versus osimertinib or afatinib [inaudible 00:29:57], for atypical mutations, for PACC mutations, et cetera. 

Dr Goldberg: All right. I think that will wrap it up. Thank you all so much. Thank you for being here.