Since lipotoxicity driven by excessive free fatty acid accumulation is a key hallmark of NAFLD, we first evaluated protein expression of TRIM56 upon exposure to PO in primary mouse hepatocytes, as well as to LPS in Kupffer cells and TGF-β1 in hepatic stellate cells (HSCs). The gene discussed is TGFB1; the disease is metabolic dysfunction-associated steatotic liver disease.