SARS-CoV-2–induced endothelial injury, along with other changes, converts normally anticoagulant endothelial cells to a procoagulant phenotype (40), leading to microvascular thrombosis and coagulopathy, and up-regulation of von Willebrand factor, all of which are clinical hallmarks of severe COVID-19 (41, –43). This evidence concerns the gene VWF and deep vein thrombosis.