Harismendy et al. demonstrated that the 9p21.3 locus alters CAD risk by modulating inflammatory signaling through altered STAT1 binding and may modify immune responses by regulating expression of IFN, a 21 or related type I IFN; and this in turn affects the expression of the cyclin-dependent kinase inhibitor gene, CDKN2A/B, which is important regulator of cell proliferation, aging, and apoptosis [13]. The gene discussed is STAT1; the disease is coronary artery disorder.