Previously, Wei et al.26 silenced AKR1B10 in MHCC97H liver cancer cells, finding that Ki-67 and the oncogenes c-myc, c-fos, and N-ras were downregulated and the pro-apoptotic protein genes caspase-3 and Bax were upregulated, indicating that AKR1B10 may promote cell proliferation, inhibit cell apoptosis, and induce hepatocyte deterioration by regulating the expression of tumor-associated genes. Here, BAX is linked to neoplasm.