Interestingly, patients with SARS-CoV-2 have been demonstrated to have increased levels of IL (interleukin)-6, IL-1β, IFN (interferon)-γ, MCP-1 (monocyte chemoattractant protein 1), MIP (macrophage inflammatory protein), and IP10 (CXCL10).11 These proinflammatory cytokines can disrupt endothelial function and integrity leading to the release of VWF, upregulation of adhesion molecules, such as ICAM (intercellular adhesion molecule)-1, integrin αvβ3, P- and E-selectin, and the production of endothelial cytokines and chemokines.56,57 Thus, the endothelium adopts a proinflammatory and procoagulant phenotype that supports the recruitment of platelets and leukocytes.58,59 Furthermore, these changes are associated with the downregulation of the natural anticoagulants and corresponding upregulation of endothelial tissue factor (TF, CD142).57 Moreover, a common finding in patients with COVID-19 is profound hypoxia. Although not formally tested in the context of SARS-CoV-2 infection, hypoxia is also likely to induce a prothrombotic endothelial phenotype since vascular hypoxia induces the activation of HIFs (hypoxia-inducible transcription factors) that have been demonstrated to upregulate endothelial TF expression while downregulating the natural anticoagulants, Protein S and TFPI (tissue factor pathway inhibitor), thus imparting a procoagulant endothelial phenotype.60