Antiplatelet drugs form the cornerstone of medical treatment in secondary prevention of arterial thrombosis. Notwithstanding the evidence that these drugs are life-saving, a quarter of the yearly arising myocardial and strokes is reoccurring [1], which suggests that current treatment is not optimal. A few years ago, combining the antiplatelet agent aspirin with a low dose of the coagulation factor Xa inhibitor rivaroxaban has been shown to be superior to aspirin alone for prevention of recurrent thrombotic events in patients with stable atherosclerotic vascular disease. The biological mechanisms underlying the overall favorable effect of this combined treatment are subject of current investigations and involve both the vessel wall and the actual thrombus forming process [2]. The clinical benefit of combined aspirin plus rivaroxaban treatment comes at a cost of more major bleeding events but not of fatal bleeding [2]. The intrinsic coagulation factor XI is considered to play a role in thrombosis but not be essential for hemostasis, i.e. the cessation of bleeding. It is therefore being regarded as a potential alternative for safer anticoagulant treatment [4].