Therefore, ADAMTS-13 and VWF imbalance may have a pivotal role in the paradigm of parenchymal extinction and liver fibrosis progression in chronic liver diseases [118,119]; indeed, the upregulation of VWF levels in the presence of chronic inflammation, vascular damage, or endotoxemia [102,103] is not counterbalanced due to the deficiency of ADAMTS-13, promoting the formation of platelet microthrombi and fibrin deposition in hepatic sinusoids, with the loss of liver parenchyma and fibrogenesis [120,121]. This evidence concerns the gene VWF and Hepatic fibrosis.