Activation of β-catenin, SMAD3-transforming growth factor-β (SMAD3-TGF-β), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), sterol regulatory element-binding protein and liver X receptor α (SREBP-LXRα) and nuclear receptor-interacting protein 1 (NRIP1), along with the inhibition of peroxisome proliferator-activated receptors (PPARs) and tumor suppressor p53 in human NASH biopsies and HCCs has been reported [4]. This evidence concerns the gene SMAD3 and metabolic dysfunction-associated steatohepatitis.