Not only hypercoagulability but also anticoagulant protein reduction contributes to thrombosis in this setting: protein C is decreased for consumption; TF pathway inhibitor (TFPI) production is impaired and is also rapidly consumed, while fibrinolysis is compromised because of endothelial PAI-1 hyperproduction stimulated by IL-1 and TNF-α [4, 5, 18]; Vrij et coll. This evidence concerns the gene TNF and thrombophilia.