From these data, we conclude that along with IR and activation of TGF-β, an important role in NASH pathogenesis is played by dysregulation of Wnt/β-catenin, NRIP1, Nrf2, SREBP-LXRα, PHBs, PPARs and p53. Here, TGFB1 is linked to metabolic dysfunction-associated steatohepatitis.