Our above findings showed that hepatic oxidative stresses were amplified by FGF1 deletion after DOX induction and our recent study indicated that Nrf2 played a pivotal role in FGF1△HBS protecting against NAFLD associated hepatic oxidative stresses [21]; therefore, we hypothesized that FGF1 deficiency might further impair Nrf2-mediated antioxidative signaling pathways under DOX treatment conditions. This evidence concerns the gene FGF1 and metabolic dysfunction-associated steatotic liver disease.