Due to the enhanced ACE activity by D allele, the production of angio-tensin II is increased which enhances degradation of cardiovascular protective agent bradykinin, this results in the local blood vessel contraction and the hypertrophy of myocardiac muscle and blood vessel smooth muscle, which causes the vessel spasm and instability of coronary artery atherosclerosis plaque, then the unstable angina or MI follows. This evidence concerns the gene ACE and coronary atherosclerosis.