In the present study, we first focused on IL-1 receptor antagonism instead of IL-6 antagonism because IL-1β signaling initiates the breakdown of the lung vascular barrier in ARDS.17 We found that the K18-hACE-2 mouse accurately modeled severe lung hyperpermeability following SARS-CoV-2 infection, similar to advanced COVID-19 patients. The gene discussed is IL1B; the disease is acute respiratory distress syndrome.