We have also observed a defect in platelet function in the annexin A7 mutant. In the platelet aggregation experiments the initial aggregation velocity was slightly, but significantly lower in platelets lacking annexin A7. These data are not reflected by a change in the in vivo bleeding time. However the reaction speed of murine platelets is much higher than those of human and due to the technical setup we might have missed larger changes in the mouse samples. The immediate reaction of mouse platelets and the absence of a lag phase after triggering may be caused by an immediately initiated thrombin generation [22]. As known from the frequent human vWF-syndrome or other haemostatic diseases, small defects often are clinically silent and do not result in physiological changes under normal conditions. Only in situations with severe physical injury, distinct environmental influences or additional platelet attributes like the platelet antigen polymorphism [53] differences might become apparent.