Finally, we leveraged genome-editing and cell-based assays to interrogate the new association signal at chromosome 19, validating the involvement of MYO9B, but also implicating another putative causal gene, HAUS8. Importantly, these experimental findings substantiate our in silico prioritization of a region with apparent regulatory influence, and our similarity-based prioritization of cell migration pathways, as both MYO9B and HAUS8 may exert their influence on CAD risk through the control of vascular cell cytoskeleton. This evidence concerns the gene HAUS8 and coronary artery disorder.