So the selected SNPs were exclusively associated with plasma HDL-C and not having pleiotropic effects on purpose
But his point was that, based on the biology, most mechanisms that increased HDL would "naturally" also reduce LDL. Thus his point was that the activity of these genes that increased HDL while leaving LDL unchanged was in some way strange. (I haven't read the paper myself, so just attempting to report my understanding of what he said - and he talked fast, with lots of big words. :)
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