Taken together, we cross-validated the data obtained in COX-2-overexpression HCC cells (Figure 3) and CRISPR/Cas9-based COX-2-knockdown HCC cells (Figure 4), and these results highlighted that the regulatory mechanism of PINK1-activated p-Drp1Ser616 mediated the functional stability of mito-COX-2/p-Drp1Ser616 interaction and its dependent mitochondrial fission, which was linked to modulating the survival phenotypes and outcomes of HCC cells in vitro (Figure 4H). The gene discussed is PTGS2; the disease is hepatocellular carcinoma.