The severity of COVID-19 is associated with host response and increased release of inflammatory mediators including cytokines and chemokines such as interleukin (IL) -2, IL-6, IL-7, IL-10, tumor necrosis factor (TNF), C-reactive protein (CRP), ferritin, and D-dimer in blood after SARS-CoV-2 replication5, these mediators promote alveolar endothelial inflammation and acute respiratory distress syndrome (ARDS)5–8. This evidence concerns the gene IL7 and acute respiratory distress syndrome.