Our studies specifically demonstrate that: (1) SULF2 transcripts are highly expressed in the liver of cirrhotic patients; (2) knockout of SULF2 ameliorates liver fibrosis in mice following BDL and treatment with CCl4 and TAA; (3) SULF2 promotes cell proliferation, cell viability, the production of collagen I(α)1, migration, and activation of HSCs; (4) SULF2 modulates the activity of the TGF-β signaling pathway in HSCs; (5) TGF-β1 forms a complex with TGFBR3 (betaglycan). Here, SULF2 is linked to Hepatic fibrosis.