CAMK2G and myocardial infarction: Murine models of myocardial CaMKII overexpression have shown ventricular dilation and hypertrophy, increased cell death, and fibrosis,109 whereas mice with genetic CaMKII inhibition are protected from left ventricular dysfunction and dilation after myocardial infarction.109 Recently, an orally available CaMKII inhibitor (RA306) has been used in mice with DCM carrying a pathogenic genetic variant in alpha-actin.