It has been shown that HSYA was able to significantly protect the liver from oxidative stress by increasing the activities of antioxidant enzymes, upregulating the expression of PPAR-γ and MMP-2, and downregulating the expression of TGF-β1 and tissue inhibitor of metalloproteinases-1 (TIMP-1), and reducing α-SMA level, which indicating that PPARγ-TGF-β1 would be a signal pathways for HSYA to reduce liver fibrosis induced by oxidative stress (Wang et al., 2013). The gene discussed is TGFB1; the disease is Hepatic fibrosis.