Thirdly, in addition to its role in activating fibrinogen, thrombin has been shown to mediate the cellular activation of macrophages, platelets and hepatic stellate cells (HSCs) via cleavage of the protease-activated receptor, PAR-1 [14, 15] and polymorphisms in the PAR-1 gene have been shown to influence rates of hepatic fibrosis [16]. This evidence concerns the gene F2R and Hepatic fibrosis.