Another mechanism is the lower concentration and biological activity of von Willebrand factor in subjects with type O blood and longer half-life and higher circulating concentrations of von Willebrand factor and factor VIII in people with blood types other than O (A, B, or AB) since it is known that severe COVID-19 infection is associated with a hypercoagulable state [10,31,32]. This evidence concerns the gene VWF and thrombophilia.