In accordance with phenotypes in Bmal1 KO mice, which displayed age-dependent dilated cardiomyopathy, BMAL1-deficient human cardiomyocytes showed characteristics of DCM including enlarged cell area, disrupted myofilament structure, increased apoptosis, attenuated contraction force, and dysfunction of calcium handling. The gene discussed is BMAL1; the disease is familial dilated cardiomyopathy.