This model presented the typical pathophysiology of MS, starting with a significant elevation in body weight, dyslipidemia, and IR until adipocyte dysfunction, which indicated the occurrence of authentic human MS39 and stimulated the incidence and progression of NAFLD-associated MS via the activation of the hepatic NF-κB/TNF-α/TGF-β1 signaling pathway. This evidence concerns the gene TGFB1 and metabolic dysfunction-associated steatotic liver disease.