This storm is the primary mechanism for ARDS responsible for mortality in patients with severe COVID-19 [3]. Previous reports had shown that patients with SARS had preferential activation of T helper (Th)-1 immunity which led to markedly elevated levels of proinflammatory cytokines (IFNγ, IL-1β, IL-6, and IL-12), which in turn leads to extensive lung damage. This evidence concerns the gene IL1B and COVID-19.