Since products of CDKN2B-AS1 promote the proliferation of vSMC, it would be logical to assume its connection with the development or progression of atherosclerosis and, therefore, CAD, but not with MI, whose main pathophysiological mechanisms are plaque rupture, erosion, erosion from calcium nodules, or intraplaque hemorrhage [15]. This evidence concerns the gene CDKN2B and coronary artery disorder.