The pathogenesis of venous thromboembolism (VTE) in cirrhosis is complex and involves several factors, both endogenous changes associated with cirrhosis with increased levels of factors VII and also protein C activity is limited in the absence of the endothelial receptor thrombomodulin and therefore it cannot exert its full anti-coagulant activity as well as external factors, one of which is limited physical activity due to the disease itself [7-10]. This evidence concerns the gene THBD and Cirrhosis.