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. This evidence concerns the gene BMAL1 and dilated cardiomyopathy.