This is despite our results suggesting that endpoints of cortical porosity and trabecular volume/structure become abnormal in hemophilia mice with complete deficiency of FVIII or FIX (and a severe defect in amplification of thrombin generation); the same endpoints are maintained in the VWF−/− mice with the severe defect of platelet associated hemostasis (combined with a mild-moderate FVIII deficiency). This evidence concerns the gene VWF and hemophilia.