These data clearly indicated that PLK-dependent TGF-β1/3 activation is induced during the pathogenesis of liver fibrosis in patients with a range of liver diseases, and that PLK-cleaved R58 LAP-DP might serve as a novel surrogate biomarker of TGF-β1/3 activation and its associated fibrosis in patients. This evidence concerns the gene PLK1 and Hepatic fibrosis.