Thrombosis can be triggered by pathological TF expression or by activation of FXII by foreign material, such as an artificial heart valve. The new generation of oral anticoagulant drugs target either FXa or thrombin. However, not surprisingly, these drugs increase the risk of hemorrhage. There is interest in FXII or FXI as new targets for safely reducing venous thrombosis. For instance, a recent study showed that reducing levels of FXI with an antisense oligonucleotide reduced venous thromboembolism (VTE) without increasing hemorrhage in patients undergoing total knee arthroplasty. VTE include deep vein thrombosis and pulmonary embolism. We are interesting in the development of new anticoagulant drugs.