Sustained and prolonged stress or injury (pressure and volume overload) leads to decompensated hypertrophy and dilated cardiomyopathy with excessive fibrosis, cardiac dysfunction, and maladaptive gene and protein expression, including an increase in CaMKII activity, TGF-β1, and collagen 1 expression [22]. Here, CAMK2G is linked to dilated cardiomyopathy.