Our previous study has shown that AKR1B10 is expressed higher in the early stages of HCC, hence we infer that NF-κB can interact with immune response molecules such as TOLL-like receptors, NOD-like receptors, directly or indirectly regulate the transcription of AKR1B10, thus affecting its expression level, jointly controlling the "chronic hepatitis—HCC" evolution. This evidence concerns the gene AKR1B10 and hepatocellular carcinoma.