Finally, the obvious characteristics of the progression of NASH to fibrosis are hepatic stellate cell activation and relatively high expression of fibrotic genes, such as transforming growth factor-β (TGF-β), α-smooth muscle actin (α-SMA), and matrix metalloproteinase-13 (MMP-13) [16]. This evidence concerns the gene TGFB1 and metabolic dysfunction-associated steatohepatitis.