Transgenic mice lacking MsrA are hyper-sensitized to CaMKII oxidation, myocyte apoptosis and structural remodeling, following a myocardial infarction while those over expressing it are protected from aldosterone mediated cardiac rupture (Erickson et al., 2008; He et al., 2011). The gene discussed is CAMK2G; the disease is myocardial infarction.