While OPN ablation was shown to reduce leptin‐induced hepatic fibrosis in vitro and in vivo,40 and ductal reaction and fibrosis in thioacetamide (TAA)‐treated mice,43 the NASH‐HCC model, which closely mirrors the full development of human disease up to HCC, reveals that NASH‐fibrosis may even exaggerate in the absence of OPN, when hyperglycaemia and lipotoxicity are the driving forces. This evidence concerns the gene LEP and hepatocellular carcinoma.