MiR-221-3p, a member of antiangiogenic gene-regulating miRNAs family and enriched in the intima layer of endothelial cells of human atherosclerotic vessels, can suppress tube formation, endothelial cell proliferation, migration and angiogenesis by inhibiting endothelial nitric oxide synthase, and facilitate the main pathophysiologic mechanisms of AMI, such as serious endothelial dysfunction, development of coronary atherosclerosis and vulnerable plaques [11, 20]. The gene discussed is NOS3; the disease is endothelial dysfunction.