Despite the fact that HGF treatment resulted in significant inhibition of key profibrogenic molecules such as Col1α1 and α-SMA mRNAs and PCNA labeling index, and upregulated PPARγ, an antifibrogenic transcription factor, HGF failed to reduce other important parameters of liver fibrosis including TGF-β1 mRNA, α-SMA labeling index, hydroxyproline content, serum ALT concentration, Sirius red-stained collagen area and fibrosis score. The gene discussed is GPT; the disease is Hepatic fibrosis.