In hearts from an adult tamoxifen-induced systemic BDNF deletion myocardial infarction (MI) model, decreased cardiac function and myocardial angiogenesis in the infarct border zone, decreased expression of the prosurvival molecule Bcl-2 and increased infarct size, cardiomyocyte apoptosis and expression of the proapoptotic molecule Bax were found compared with those in wild-type MI hearts. This evidence concerns the gene BAX and myocardial infarction.