In contrast, mice with transgenic myocardial overexpression of AC3-I, a peptide inhibitor active against all CaMKII isoforms, are protected against a host of myocardial insults, including myocardial infarction (20, 125), calcineurin overexpression (126), inflammation (46, 117), infusion of isoproterenol (21, 125), angiotensin II (21), and aldosterone (20). Here, CAMK2G is linked to myocardial infarction.