 Liver cirrhosis has traditionally been seen as a state of hypocoagulability and can be protected against thrombosis. However, recent studies have completely changed this paradigm. Patients with liver cirrhosis have an impaired hepatic synthesis of procoagulation factors but also anticoagulation factors, which is associated with an increase in other procoagulant factors such as factor VIII and von Willebrand factor which determines an elevated thrombin generation and, ultimately, a hypercoagulability state. Several consequences of hypercoagulability can be expected, such as portal vein thrombosis and venous thromboembolism. In addition to the potential direct deleterious consequences for the development of portal vein thrombosis, recent data have shown a close relationship between the activation of coagulation and faster progression of liver fibrosis. 