One of the principle mechanisms for the anti-apoptotic effects of cardiac β-arrestin2 is transactivation of the epidermal growth factor receptor (EGFR) by the cardiac β1AR [53], which is exclusive for β-arrestin2 because β-arrestin1 does not stimulate this; instead, it promotes cardiac apoptosis post-MI (Figure 1) [53,60]. This evidence concerns the gene EGFR and myocardial infarction.