We further discovered that BMAL1 binds to the E-box element in the promoter region of the mitochondrial gene BNIP3. Knocking out BMAL1 caused a decrease in BNIP3 protein expression, which partly induced impaired mitochondrial fission and mitophagy, leading to compromised cardiomyocyte function and the macroscopic phenotype of DCM. The gene discussed is BNIP3; the disease is familial dilated cardiomyopathy.