Excessive CaMKII activation is critically involved in multiple cardiac pathological conditions, such as myocardial ischemic injury (12–15), arrhythmia (16, 17), cardiac hypertrophy and remodeling (18, 19), and cardiomyopathy and heart failure (15, 19), and inhibition of CaMKII over-activation profoundly alleviates these cardiac diseases in animal models (13–15, 19–23). This evidence concerns the gene CAMK2G and cardiac hypertrophy.