BAK1 and myocardial infarction: The following findings that support a close relationship between Bcl-2 and mPTPC were observed in cells/mice deficient in Bax and Bak: (1) mPTP-induced cell death and related mitochondrial damage is inhibited in cardiac cells after a myocardial infarction [259]; (2) mitochondria are resistant to the opening of mPTP; (3) reconstitution of Bax in such cells restored both the mPTP opening [258,259] and outer mitochondrial membrane permeability [258]; and (4) Bax/Bak deficiency is protective regarding the conditions of ischemia-reperfusion injury [258,259].