HSCs are crucial for development of liver fibrogenesis; their depletion leads to marked amelioration of fibrogenesis and, downregulation of MFB-like cell markers following chronic liver injury.29 Hence, developing anti-fibrotic therapies to treat hepatic fibrosis/cirrhosis can potentially decrease morbidity and mortality in patients with chronic liver diseases30 who are at risk for hepatocellular carcinoma.31 This study identifies the t-PA/LRP1 ligand/receptor pair on activated HSCs as potential new targets for anti-fibrotic therapies. This evidence concerns the gene PLAT and hepatocellular carcinoma.