Indeed, several prothrombotic hemostatic mediators are elevated, including fibrinogen, soluble thrombomodulin, soluble TF, thrombin–antithrombin TAT complex, von Willebrand factor, Factor VIII, and C-reactive protein (CRP).2, 12The generalized inflammatory state, the endothelial dysfunction, and possibly poor clearance of some of the thrombotic mediators may account for this derangement.5 This evidence concerns the gene CRP and endothelial dysfunction.