Protein C (PC) is a vitamin K-dependent plasma protein which is synthesized in the liver. It is a physiological inhibitor of the coagulation cascade which, together with Protein S, cleaves the activated forms of Factors V and VIII. PC also promotes fibrinolysis by activating Plasminogen Activator Inhibitor (PAI). The main purpose of testing for inhibitors of coagulation is to detect congenital deficiency. Congenital PC deficiency can be either qualitative or quantitative with autosomal dominant or autosomal recessive transmission. Congenital PC deficiency is more common than congenital antithrombin III deficiency and is associated with venous thrombosis, thromboembolism and, less commonly, arterial thrombosis. There are two types of Protein C deficiencies: type 1 is related to quantity and type 2 to abnormal function. Causes of acquired protein C DEFICIENCY include: acute thrombosis, warfarin therapy, liver disease, vitamin K deficiency, sepsis, Disseminated intravascular coagulation (DIC), and certain chemotherapeutic agents (eg, L-asparaginase). PC levels can RISE in a variety of circumstances, including pregnancy, coronary heart disease, diabetes, nephrotic syndrome and in patients taking oral contraceptives.