In acute infection, patients with severe COVID-19 had higher levels of cGAS, STING, IFN-α, TNF-α and IL-6 expression than patients with nonsevere manifestations of the disease, demonstrating that cGAS and STING activation, which is responsible for inducing IFN-I and proinflammatory cytokine production, contributes to the maintenance of an intense systemic inflammatory state characteristic of severe COVID-19. The gene discussed is IFNA1; the disease is COVID-19.