In summary, we demonstrate here 1) PLK cleaves LAP between R58 and L59 residues, 2) PLK-dependent TGF-β activation occurs in human hepatic fibrosis, and 3) PLK-cleaved LAP-DP is the potential surrogate marker for proteolytic TGF-β1/3 activation and in turn fibrogenesis in the liver. The gene discussed is PLK1; the disease is Hepatic fibrosis.