Thirdly, they indicate that targeted deletion of the AKAP2 gene in adult cardiomyocytes increases myocardial apoptosis, reduces new vessel formation and exacerbates cardiac dysfunction associated with MI, thus suggesting that AKAP2 functions as a coordinator of cardioprotective signals that attenuate myocardial damage in infarcted hearts. This evidence concerns the gene PALM2AKAP2 and myocardial infarction.