HSYA significantly reduced liver fibrosis via downregulation of α-smooth muscle actin (SMA), collagen α type I, matrix metalloproteinases (MMP)-9, and tissue inhibitors of metalloproteinases (TIMP)-1, associated with decreased expression of transforming growth factor (TGF)-β1 and phosphorylation of Smad4[25], and upregulation of the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) and matrix metallopeptidases-2 (MMP-2)[26,27]. The gene discussed is MMP2; the disease is Hepatic fibrosis.