In conclusion (Fig. 6), this study demonstrates that DRP1-mediated mitochondrial fission and mitophagy are activated in hypoxia-surviving HCC cells to attenuate apoptosis, and targeting DRP1-mediated mitochondrial fission and subsequent mitophagy increases mitochondrial apoptosis of HCC cells during hypoxia, suggesting a new approach to enhance the embolic efficacy of TAE/TACE treatment. Here, DNM1L is linked to hepatocellular carcinoma.