In the pathogenesis of severe coagulation abnormalities in sepsis, three major mechanisms are supposed to play a role: the tissue-factor driven accumulation of thrombin with subsequent fibrinogen conversion, binding to the platelet surface receptor GPIIb-IIIa, and, finally, platelet activation and clotting; impairment of the anti-thrombin, protein C and tissue factor pathway inhibitor anti-coagulative systems; and inhibition of fibrinolysis by increased PAI-1 production [31]. Here, SERPINE1 is linked to Sepsis.