Animal models support that deficiency of FXI or FXII, or the inhibition of these proteases by different compounds strongly protect against venous or arterial thrombosis without risk of bleeding (9), and a clinical trial using anti-FXI oligonucleotides demonstrates a better antithrombotic efficacy and lower risk of bleeding than classical anticoagulants (heparin) (26). Here, F11 is linked to Arterial thrombosis.