We and others have shown that chronically activated cardiac NF-κB, JNK pathways, impaired insulin signaling-induced metabolic disturbances, dysregulated calcium homeostasis and an over-activated renin-angiotensin system are emerging as major molecular and metabolic mechanisms for DCM [3,4,5,6,7,8]. The gene discussed is MAPK8; the disease is familial dilated cardiomyopathy.