Given the lack of effect of increased mitochondrial CaMKII activity on myocyte survival, mitochondrial Ca2+, ROS, or ΔΨmito, activators and measures of the mitochondrial transition pore (mPTP) opening, we did not anticipate mPTP was involved in the dilated cardiomyopathy present in mtCaMKII hearts. The gene discussed is CAMK2G; the disease is dilated cardiomyopathy.