HSCs from p47phox-deficient mice (without a regulatory component of NOX) fail to generate ROS in response to angiotensin II, platelet derived growth factor (PDGF), leptin, or apoptotic bodies, and p47phox-deficient mice demonstrate reduced liver fibrosis after BDL or the hepatotoxin CCl4. This evidence concerns the gene NCF1 and Hepatic fibrosis.