ABHD2 and coronary artery disorder: In vitro deletion of this intergenic region by CRISPR–Cas9 increases MFGE8 expression—with no change to ABHD2 expression—and MFGE8 knock-down reduces coronary artery (CA)-VSMC and monocyte (THP-1) proliferation, lending functional support to MFGE8 as a likely causal mediator of the CAD association in this region44.