For the mechanism, DRP1 blockage induced a significant mitochondrial accumulation of Bax (Fig. 2f), a classical inducer of mitochondrial permeability transition, resulting in a massive cytochrome c and AIF release from the mitochondria to the cytosol, and an increased activation of cleaved caspase-3 (Fig. 2f), suggesting that DRP1 inhibition increases mitochondrial apoptosis of HCC cells during hypoxia. This evidence concerns the gene DNM1L and hepatocellular carcinoma.