TGFB1 and Hepatic fibrosis: Quiescent HSCs can rapidly differentiate into myofibroblast with increased extracellular matrix (ECM) synthesis and deposition in response to fibrogenic stimuli, including transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) (Liu et al., 2006; Inagaki and Okazaki, 2007), so activated HSCs are central to the pathogenesis of hepatic fibrosis.