Some evidence indicates that FVIII has greater affinity for VWF than polyP: (i) in normal individuals, in whom levels of circulating FVIII are 40–50 times lower than VWF [27], there is no activating effect of polyP on VWF, and (ii) polyP activates VWF more efficiently in those cases when FVIII levels are extremely low, such as in severe hemophilia A and in type 3 VWD. This evidence concerns the gene VWF and von Willebrand disease 3.