Von Willebrand Factor (VWF) plays a role in the maintenance of hemostasis, where 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. It 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. Defects in VWF are the cause of von Willebrand disease (VWD), a group of hemorrhagic disorders in which the von Willebrand factor is either quantitatively or qualitatively abnormal, resulting in altered platelet function. Symptoms vary depending on severity and disease type but may include prolonged bleeding time, deficiency of factor VIII and impaired platelet adhesion.