Similarly to cirrhosis, vWF and ADAMTS-13 levels and the impaired physiological functions associated with them seem to be associated with HCC and portal hypertension not only through the stimulation of fibrogenesis, as previously discussed, but also through the induction of angiogenesis, promoting VEGF Receptor 2 phosphorylation, which enhances VEGF expression. Here, VWF is linked to hepatocellular carcinoma.