In this context and because rFVIIa may increase the risk of arterial thrombosis [31], we speculate that using excess rFVIIa in off-label indications combined with TF generated in disrupted or inflamed atheromas or other clinical conditions can induce thrombotic events, since the TF-FVIIa complex drives the intrinsic coagulation pathway to form thrombin and fibrin [32]. This evidence concerns the gene TF and Venous thrombosis.