VWF is important in hemostasis, and genetic defects in the structure and modification of VWF can cause von Willebrand disease (VWD), the most common congenital bleeding disorder in humans. Important in the maintenance of hemostasis, it promotes adhesion of platelets to the sites of vascular injury by forming a molecular bridge between sub-endothelial collagen matrix and platelet- surface receptor complex GPIb-IX-V. Also acts as a chaperone for coagulation factor VIII, delivering it to the site of injury, stabilizing its heterodimeric structure and protecting it from premature clearance from plasma.