Interestingly, type I IFN responses coexisted with TNF- and IL-1β-driven inflammatory responses in classical monocytes from severe COVID-19 patients but not in those from mild COVID-19 patients, indicating that type I IFNs contribute to exacerbation of TNF- and IL-1β-driven inflammation during the development of severe COVID-19. The gene discussed is IL1B; the disease is COVID-19.