After SARS-CoV-2 infection, a large number of signal responses are induced within the lungs, followed by the release of cytokines and chemokines such as IL-1β, IL-6, IL-8, CXCL10, and TNF-α, and the recruitment of inflammatory cells to the infected sites, which often leads to acute respiratory distress syndrome (ARDS), multiple organ failure, and even death [2, 3]. This evidence concerns the gene IL1B and acute respiratory distress syndrome.