However, mtCaMKII mice, burdened by chronic, pathological elevation in mitochondrial CaMKII, exhibit loss of CKmito and complex I that prevent this metabolic benefit, and instead contribute to metabolic insufficiency, elevated diastolic cytoplasmic [Ca2+], and severe dilated cardiomyopathy. The gene discussed is CAMK2G; the disease is dilated cardiomyopathy.