The most convincing data were: (i) the demonstration that tissue factor expression in circulating leukocytes can be stimulated by pathogens; (ii) an acquired deficiency of endogenous anticoagulant proteins such as antithrombin and protein C in sepsis patients; and (iii) a sustained increase in fibrinolysis inhibitors such as PAI-1, resulting in hypofibrinolysis [30]. The gene discussed is SERPINE1; the disease is Sepsis.