AKR1B10 induction by specific factors was postulated to promote HCC cell proliferation through the depletion of retinoic acid in the early stages of primary HCC, however in advanced HCC, this pathway becomes inactivated, resulting in the downregulation of AKR1B10 (by other as-yet unknown factors) and leading to EMT and tumor metastasis. This evidence concerns the gene AKR1B10 and neoplasm.