The exogenous addition of the HCV NS3 protease to cultured hepatocytes led to increased expression of collagen I, TGF-β1, and TGF-β type I receptor [73]; additionally, NS3 directly interacted with the TGF-β type I receptor at the surface of HCV-infected cells and in HCV-infected chimeric mice, an anti-NS3 antibody attenuated HCV-induced liver fibrosis. Here, TGFB1 is linked to Hepatic fibrosis.