There is emerging evidence that that heightened activation of endothelial cells, causing the release of large von Willebrand factor (VWF) multimers, in combination with insufficient VWF cleavage due to ADAMTS13 consumption or disease pathophysiology related to COVID-19, might lead to escalated interactions between platelets and vessel walls, ultimately resulting in thrombotic microangiopathy [156]. This evidence concerns the gene ADAMTS13 and thrombotic microangiopathy.