Although TGFB1 has not been identified as the causal gene in this locus through mechanistic studies, and there are not highly informative eQTLs in vascular cells or tissues, algorithms that integrate available gene expression and CAD association data, Summary data-based Mendelian Randomization [66] and MetaXcan [67], provide compelling support for the causality of TGFB1. These data suggest that TGFB1 expression promotes CAD risk, which is consistent with the fact that canonical TGFβ1 signaling occurs primarily through the risk-promoting SMAD3 pathway. Here, SMAD3 is linked to coronary artery disorder.