The fibrinogen molecule is becoming increasingly understood. Amino acid sequencing has been undertaken and studies of abnormal fibrinogens are leading to a more functional concept of its structure. Acquired dysfibrinogenemia appears to be a more common problem than previously thought, and may be found in patients with liver disease, cancer, fibrinolysis, and disseminated intravascular coagulation (DIC). While previous evidence suggested that anti-thrombin activity and fibrin polymerization inhibitors were formed in these conditions, recent studies suggest that slow fibrin formation occurs as a result of structural changes induced in the fibrinogen molecule itself. These relatively minor, alterations in structure cause a functional dysfibrinogenemia simulating abnormalities seen in some congenital fibrinogenopathies. A case is presented illustrating such a dysfibrinogenemia in a patient with cirrhosis of the liver and evidence for DIC.