Furthermore, the positive correlation between the concentration of platelet aggregates and the vascular endothelial dysfunction characterized by the VWF:RCo, FVIII, and TM levels (Fig. 5a) is aligned with the currently accepted theory of the pathophysiological mechanism of COVID-19 in which the viral entry into host cells is mediated by the ACE2 receptor, causing vascular endothelial damage and resulting in endothelial vascular dysfunction and vasculitis (i.e., the inflammation of blood vessels)2,6. This evidence concerns the gene F8 and vasculitis.