During heart failure, CaMKII (in the human heart, mainly CaMKII-δ9) was activated by multiple cardiac pathological insults, including neurohumoral agonist signaling (43), oxidant stress (44–47), hyperglycemia (48, 49), ischemic injury (12, 13, 50–52), cardiac toxic drugs (12, 53), and other adverse stimuli associated with increased intracellular calcium levels (54, 55). This evidence concerns the gene CAMK2G and heart failure.