Collectively these GRN data, which are agnostic to the GWAS SNPs in the HDAC9-associated CAD risk locus, confirm that both HDAC9 and TWIST1 are likely involved in the pathogenesis of CAD, but also suggest an additional key driver role for TWIST1 in GRN 116 in SKLM. This evidence concerns the gene HDAC9 and coronary artery disorder.