DNM1L and hepatocellular carcinoma: Mechanistically, DRP1 inhibition increased mitochondrial translocation of pro-apoptotic protein Bax, resulting in the loss of mitochondrial membrane potential and abundant release of AIF and cytochrome c from mitochondria to the cytosol to trigger mitochondrial apoptosis of hypoxic HCC cells, thereby enhancing hypoxic cytotoxicity to HCC cells.