In this study, we did not observe a significant increase in VWF in the supernatant of vascular organoids treated with viral antigens, suggesting that VWF release associated with endothelial activation may result from the dysregulated immune/inflammatory response associated with SARS-CoV-2 infection rather than pericyte or EC infection.50–54 With the lack of efficacy of anti-platelet drugs in improving outcome in severe COVID-19 patients38,55,56 endothelial activation and release of VWF represents a potential target to limit thrombosis in COVID-19 patients. This evidence concerns the gene VWF and infection.