In addition to the previously reported profibrotic factors such as transforming growth factor-β (TGFβ) and platelet-derived growth factor, the study of fibroblasts in NASH may elucidate specific pathways activated in metabolic stress-induced liver fibrosis, and thus gives insights into the molecular mechanisms underlying liver fibrosis-mediated HCC development. The gene discussed is TGFB1; the disease is metabolic dysfunction-associated steatohepatitis.