In contrast to the dilated cardiomyopathy and near normal lifespan in mtCaMKII mice (Fig. 1l), myocardial CaMKII overexpression in the absence of subcellular targeting causes marked cardiac hypertrophy, left ventricular dilation, increased myocardial cell death, cardiac fibrosis, heart failure, and premature death12,13. Here, CAMK2G is linked to heart failure.