Indeed, the notion that a VWF-mutant unable to bind αIIbβ3 is protective against thrombosis in a ferric chloride-induced model for arterial thrombosis while it is without effect in a stroke model, is a perfect example of this constant reassessment that is forced upon us.100,186 The possibility to target VWF in the management of thrombotic disorders should therefore be considered as a real option. This evidence concerns the gene VWF and stroke disorder.