These results showed that 3 days after myocardial infarction, the expression level of Bcl‐2 in AMI model group was significantly repressed, accompanied by the upregulation of Bax and increased apoptosis index of myocardial cells, indicating that Bcl‐2/BAX is an important pathway to induce apoptosis of myocardial cells. This evidence concerns the gene BCL2 and myocardial infarction.