Notably, disruption of DRP1 activity by pharmacologic inhibitor Mdivi-1 (an effective DRP1 inhibitor, inhibiting mitochondrial fission) or genetic knockdown suppressed mitochondrial fragmentation and hypoxia-induced mitophagy, resulting in a significant increase of mitochondrial apoptosis of hypoxic HCC cells, potentiating cytotoxic hypoxia to HCC cells. The gene discussed is DNM1L; the disease is hepatocellular carcinoma.