Comparing different animal models of lean NAFLD, the most common mechanisms of liver fibrosis include the overexpression of TGF-β, α-SMA, and collagen type I. Additional factors that contribute to liver fibrogenesis in lean NAFLD models include MMPs, TIMPs, PPARγ, TLR2, and TLR4 and the overactivation of HSCs. This evidence concerns the gene TGFB1 and metabolic dysfunction-associated steatotic liver disease.