In most patients with acute or chronic liver failure, extensive changes in all pathways contributing to hemostasis are found. These hemostatic alterations concern both pro- and antihemostatic pathways, and therefore the net result of the hemostatic dysbalance is unclear. Although it is generally believed that patients with liver disease have a hemostasis-related bleeding tendency, this concept is challenged in recent literature. Although the bleeding problems in patients with liver disease are obvious, the clinically most relevant bleeding episodes, i.e., bleeding from ruptured varices or ulcers, are due to vascular abnormalities and portal hypertension, and not to an abnormal hemostatic system. Moreover, patients with liver disease sometimes experience thrombosis of the portal vein or hepatic artery, which is in part attributed to hypercoagulation. In addition, a substantial part of the patients with liver disease undergoing liver transplantation can nowadays undergo this major surgical procedure, which involves significant hemostatic challenges, without transfusion of blood products. Therefore, the recent debate on the presence of a major hemostatic defect in patients with liver disease seems justified. This paper will review the hemostatic changes that occur in acute and chronic liver failure, and will review hemostasis testing and reversal of coagulopathy in these patients.