In vitro, LPS-stimulated human monocytes inhibit fibrinolysis through a tissue factor-mediated enhancement of TAFI activation and make clots resistant to the profibrinolytic activity of heparins.119 Because TF-expressing monocytes-macrophages drive blood clotting activation in sepsis, our findings provide an additional mechanism whereby these cells may favor fibrin accumulation in the microcirculation. Here, TF is linked to Sepsis.