Every time we make a great molecular finding, we bump into a clinician that had the intuition for many years that something like that was going on. So, I think my communication to the clinical field would be when you have an intuition that something is going on, find a basic researcher that's doing research close to that, reach out to them and tell them about it. Because often in basic research, we're so far away from the patients that we also treat the disease as one lump. One simple thing. But we know that every patient is different and in the end we want to do precision medicine. Hi, I'm Andrew Pospisilik. I'm a full professor and Chair of the Department of Epigenetics at the Van Andel Institute. I'm a diabetologist from the basic research side, so I don't see patients. I'm a PhD, and I study metabolic diseases, I study endocrinology, and epigenetics. Epigenetics are the molecular mechanisms that control cell identity and that control how our genes are expressed and when. So, they're really at the heart of function of any cell type. And this is done by a set of proteins that regulates how DNA, which is wrapped around histones, is compacted and kind of put out of commission and into the closet, so that genes can't be expressed or opened up, so that they can be expressed. One of the big findings we've made in the epigenetics space is that there are probably two different types of beta cells, one that have very strong epigenetic control and one that have weaker. And so, just like having beta cells and alpha cells gives us functional compartmentalisation of endocrinology in the human, one that raises glucose, one that lowers it, having two different beta cell subtypes means that we probably have functional compartmentalisation about how appropriately we secrete insulin, so how quickly it's secreted. And because we see that one of these beta cell subtypes is more proliferative than the other, it probably will become really important in the compensatory response to whether it's high-fat diet or diabetes, as the beta cell compartment tries to expand and accommodate metabolic stresses. Being able to manipulate the ratio of these two cell types or being able to stimulate one or the other cell type to grow in its compartment has a lot of therapeutic implications. 52 I think, epigenetics has a lot of potential for understanding the origins of heterogeneity, and that's both at the cellular level, so I talked about different beta cell subtypes that we've identified through epigenetic heterogeneity, but at the same time different human subsets. So, if we talk about diabetes, for instance, it’s one of the pioneering fields that have described what we call disease endotypes, subtypes of disease that are driven by different molecular underpinnings. We have evidence that there's at least two major types of obesity, for instance, one of them seems to be epigenetically driven. So, this is like an epigenetic or developmental endotype of obesity. That's still nowhere near the clinic. We still don't have the diagnostics for what markers definitively demonstrate that an individual is, we've called it type A or B obesity for now, but there's definitely very strong epigenetic differences between those two classes. And those two classes of obesity are definitely also highly correlated with sort of healthy and unhealthy obesity. So it could be that a lot of the healthy versus unhealthy obesity in the populations around us are driven very much by epigenetic origins. Take home messages or conclusions: There's nothing to replace the wisdom and experience in the clinic, right? Every time we make a great molecular finding, we bump into a clinician that had the intuition for many years that something like that was going on. So, I think my communication to the clinical field would be when you have an intuition that something is going on, find a basic researcher that's doing research close to that, reach out to them and tell them about it. Because often in basic research, we're so far away from the patients that we also treat the disease as one lump. One simple thing. But we know that every patient is different, and in the end we want to do precision medicine, right? We want to treat every patient as well as possible.