Thanks Xiangyu, that makes sense but it’s not quite what I’m after.
A part of this ask that is less typical is that I’m solely concerned with coding associations. I would be fine taking putative LoF variants or in silico functionalizations, e.g. from Sei, of missense variants (as GoF or LoF) as indications of how these variants effect the gene they code for.
This is a vastly smaller pool of variants I’m talking about, but they’re far more predictive of clinical outcomes, much easier to infer causality for and there are quite a lot of them now so I’m seeing what I think is a good reason in the near future to start trying to connect them to implied therapeutics. The “in silico functionalization” bit is still perhaps questionable, but that’s a part of why I was wondering if this is on the radar for you all. Or perhaps you all know of much better ways to do this or pitfalls with the combination I’m proposing?
Maybe @ochoa and/or @MayaGhoussaini have done research in this direction already?