In turn, the association found between viral RNA load in plasma and three mediators of endothelial dysfunction (VCAM-1, angiopoietin-2 and ICAM-1), and with coagulation activation markers (D-dimers and INR prolongation) suggests a potential virally linked mechanism in the pathogenesis of endotheliitis and thrombosis in COVID-19 disease [7]. This evidence concerns the gene VCAM1 and deep vein thrombosis.