Lung vascular hyperpermeability is the primary cause of protein-rich edema formation in lungs leading to ARDS and ultimately to death due to defective gas exchange in the fluid-filled alveoli.3 To address whether IL-1β–induced downregulation of VE-cadherin could underpin lung vascular hyperpermeability observed in SARS-CoV-2 infection in mice, we investigated the therapeutic potential of the IL-1RA anakinra.27 K18-hACE-2 mice received anakinra (10 mg/kg per day, IP [intraperitoneal]) 24 hours after the sublethal dose of SARS-CoV-2 (2×104 p.f.u.)and thereafter, daily injections (Figure 4A). The gene discussed is IL1B; the disease is acute respiratory distress syndrome.