IL-1R antagonism prevented the IL-1β–mediated decrease in expression of the endothelial junctional protein VE-cadherin, which maintains the integrity of endothelial adherens junctions.68 The excessive generation of proinflammatory cytokines such as IL-1β during the cytokine storm described in severe SARS-CoV-2 infection10–12 likely leads to widespread VE-cadherin downregulation in lungs and thus explains the high incidence of pulmonary edema and respiratory failure in severe COVID-19 patients. This evidence concerns the gene IL1R1 and COVID-19.