Degradation of normal liver ECM contributes to the pathogenesis of liver fibrosis, particularly in the early stages of injury [36].The ameliorated disease development in MMP19KOs likely originates from slower kinetics of basement membrane destruction and ECM remodeling, as MMP-19 is known to process a number of basement membrane proteins such laminin 2γ chain, tenascin C, collagen IV, and nidogen-1, which all are abundant components of normal liver ECM [20], [22], [23]. This evidence concerns the gene MMP19 and Hepatic fibrosis.