 Thanks, Gail. So I'm here just representing the committee, and let me also say that this is a work in progress, and so I'm glad that we have this on the agenda to get lots of feedback in terms of how to continue making this better. To many of you know, this discussion started out in 2013 with the first publication in terms of how to think about incidental findings, so-called at the time, and eventually revised to be called secondary findings in the sense that we were going to intentionally look at exomes and genomes for these at the time, 56 genes. There was a revision in 2014 that many of you were part of in terms of giving the ability to opt out of that, and the getting feedback from the community, we realized that this was going to be both an evolving field, and perhaps that 56 was not ultimately going to be exactly right, and we wanted to have a way of being able to modify this over time, and this is the first of what I'm sure will be several revisions, but 2.0 in terms of this, and this recently came out in genetics and medicine at the end of 2016. So the American College of Medical Genetics put together a committee to be able to vet both to think about the genes that were on the list, whether or not they should all be on the list, and more importantly, perhaps, to think about whether or not other genes needed to be on the list. One thing I think we learned from the first committee was that we needed to have broader input from the community, so not just members, for instance, from the American College of Medical Genetics, but also individuals, for instance, from AMP representing also the cardiology community, the oncology community. So we had more sort of diversity on the working committee as we thought about this. As we tried to think about the evidence, and we really did try and use evidence for all of this, we used evidence both in the genomic dimension in terms of what we knew about mutations. Thankfully, ClinVar was up and running by the time we were doing this, so we had a lot of evidence to come from that, as well as the evidence that was coming through ClinGen at the same time that was set up, and I'll explain that in just a second. So as we thought about the criteria for all of these, this was meant to be a nomination process where people from the community could be able to nominate genes in or off the list as we were doing this, and again, thinking about the criteria, thinking about both how common the conditions were, what the clinical features were, and how actionable this information was. After this information was nominated by any members at large, and we actually solicited very specifically input from many of the different societies. You probably either just deleted some of these messages or they went into your spam box, but we did try and get broad input from the community. The committee reviewed the worksheets that people, nominators filled out to go with this. When we needed to, we brought in experts, when we needed to have subject domain expert on this, and ultimately the board of the American College of Medical Genetics voted on this to approve what was eventually accepted. So as we did this, some of the criteria that we used were thinking about the severity of the condition. We wanted it to be a serious condition with a high probability or a high enough probability, or in other words, that the penetrance was high enough that actually the health threat would materialize, that there was actually effective intervention for all of this, and that we had good evidence about the strength of that effectiveness of the intervention, and that whatever the intervention was would be acceptable in terms of the participants that would get this information. As I said, and I want to give credit to Jim and Katrina. The ClinGen Actionability Working Group, again, was evolving at the same time, and so we actually begged, borrowed, and took from all of the work that they had been doing so that we didn't have to reinvent the wheel in terms of actionability for these conditions. Oh, okay. So in terms of this, what eventually, just to get to the punchline, we took one gene off the list and added four genes to the list, and I'll go through these in detail. These weren't radical changes, and I have to say we were somewhat disappointed that we didn't get more feedback from the community, so this is very much a call to action for all of you guys, and I know this is part of what we'll spend some time doing, but please, please, please, we want to be able to evaluate more conditions as we're thinking about this. So just going through this very quickly, the one gene that we have taken off the list was milk. This is one of the, I would argue, very rare causes for thoracic abdominal aortic aneurysms, and I'll get into why we took that off the list in a second, but two that we added were forms of juvenile polyposis, so within the lines of thinking about the Lynch syndrome genes, they sort of fit into that category, as well as two inborn errors of metabolism, Wilson's disease and OTC, ornithine transcarbamylase deficiency. Again, I won't go into detail on this, but for those of you who are familiar with ClinGen, this is actually the actionability criteria that were used and they used in terms of thinking about these things, the severity of the condition, again, the likelihood of disease, the efficacy of intervention, and then what the nature of that intervention is. So just very quickly at a high level, and then I'll go through each one of these for juvenile polyposis. There were two genes that were added, BMPR1A as well as SMAD4, and really we thought about those very much together because they're more like than they are different. Wilson's disease, as many of you know, a copper storage disease, ornithine transcarbamylase deficiency, or urea cycle defect, which is X-linked and important to remember, and then the one gene being taken off milk. And again, one of the issues that came up very specifically with milk was the rarity of pathogenic variants. And remember, we have a relatively high level of evidence or relatively high threshold, I should say, in terms of returning pathogenic or known pathogenic variants. And in fact, and I just checked again in ClinVar this morning, really almost all of the mutations that are seen within milk are either copy number variants, which are the vast majority. There are actually only two known pathogenic mutations that are reported within ClinVar, one of which, and only one of which, I should say, has been seen by a clinical laboratory. So it was really in terms of the likelihood of finding something, that was a big part of why we took that off the list. So in terms of juvenile polyposis, again, two genes here. The penetrance was felt to be very high based on the evidence, penetrance in some cases as high as 70%, basically by age 70. This is something, for those of you that may not be familiar with the condition, increases the risk of both colon cancer as well as gastric cancer. The polyps themselves, it's called juvenile polyposis because of the pathology of the polyps themselves, not because necessarily you get these when you're a juvenile, although you do tend to start the polyposis, seeing these polyposes at an early age. This is something also in terms of confirming that this really is a disease-associated variant. Many times those polyps are obvious either with colonoscopy or endoscopy, and again, the pathology being so distinctive, there's actually a very good likelihood of being able to get, if you will, a physiologic readout that the molecular prediction is in fact correct. And again, this is something that for many individuals, relatively early age of onset where we wouldn't be doing, for instance, colonoscopies, endoscopies at the age we would need to starting, for instance, even into the 20s or 30s. Well, since disease, again, a copper overload disorder, important because this is a progressive disorder, it actually has a very effective therapy in terms of chelation. The symptoms may go for many years undiagnosed because they can be amorphous. And importantly, there are orthogonal ways of being able to confirm the diagnosis. So being able to, once you make the molecular diagnosis, being able to look at ceruloplasm, 24-hour copper urine, there are ways of orthogonally confirming this. And so again, and those are relatively easy, non-invasive tests to be able to do this. So that was part of the rationale for thinking about this. Ornithine transcarbamylase deficiency, again, this is an X-link disorder, so there are some differences between males and females for this condition. As a ureocycle disorder, very, very severe in terms of literally, you know, seizures, coma, death. It can be the progression with this type of disorder, especially in males. But even in females, 20 to 30% of these women can be manifesting, and especially under stressful conditions, protein overload, catabolism, pregnancy, other things that can bring out or stress the system for these. Many times undiagnosed, especially if an ammonia is not sought. And so it was important we thought to be able to raise awareness of this. This is something that's part of newborn screening, but again, this is something for females if they weren't part of newborn screening at the time, or manifesting females may not have been diagnosed, and this is again something where combination of dietary modification, as well as in acute situations, essentially we can take off the ammonia with using other ways of bypassing the ureocycle and being in one necessary dialysis. So thought to be quite helpful in terms of that. I'll just spend one second, again, on milk. Again, this was the one gene that was taken off the list, and this was in large part because amongst the laboratories, and we had good representation for the laboratories, they were spending a lot of time vetting variants of uncertain significance within this. Again, whenever one of these genes comes on the list, the laboratories feel an obligation to be able to vet all the variants that they were seeing and in the yield, if you will, from this just wasn't extremely high. From the clinical point of view, one of the concerns about this was that unlike, for instance, fibrillin mutations, you don't always see, in fact, you don't often see a presymptomatic stage where you're seeing aortic dilatation at a time when you can then intervene effectively for this. So we didn't have an orthogonal, if you will, physiological biomarker or something to be able to confirm the variants that we were seeing as well as knowing that we had this stage or this period at which you could know that you could intervene effectively because, for instance, you were seeing disease progression and might need to go in and do surgery or start medication. And so for that reason, milk was taken off the list. I just wanna give credit, especially to Sarah, who was the first author on this paper, but the entire group, Christa Martin, David Miller were the chairs for this committee and I think we're gonna take a question now or we're gonna save up. Okay, so I'll take a question now, Mark. Yeah, right. So I lost over this, but thanks, Mark, for the point. So in addition, HHT is another manifestation of SMAD4. It was something that we actually have in the paper for those of you who take the time to read it to be able to see that as another. We actually didn't use that to upgrade, if you will, so the decision was made solely based on the juvenile polyposis, but it's sort of a bonus in terms of being able to get that information as well. Okay, so we will move on to Sharon.