Increased levels of vWF, which is an endothelial adhesion protein, were reported in both COVID-19 patients who were treated in intensive care units and in patients who did not fall into critical condition, and this increase was associated with the decreased activity of a disintegrin and a metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), a metalloproteinase that regulates the size of the vWF multimer [37,38]. This evidence concerns the gene VWF and COVID-19.