Moreover, in vitro and in vivo data showed that transplantation of integrin β1 overexpression-modified BMSCs significantly increased the adhesion of BMSCs and protected cardiomyocytes in a rat model of MI, inhibited apoptosis and regulated cell survival signaling by activating FAK and ILK, as evidenced by a decrease in the expression of the pro-apoptotic proteins cystein-3 and bax, and a significant increase in the expression of anti-apoptotic proteins such as bcl-2 in the myocardium, thereby contributing to angiogenesis and cardiac survival (55). The gene discussed is BCL2; the disease is myocardial infarction.