As mammalian IFN-α and IFN-λ2/3 subtypes evolve more inductive and antiviral activity than the epithelial-specific IFN subtypes (such as IFN-β and IFN-λ1) [49,50], the robust reaction of inflammatory IFN responses via recruited immune cells in the lung certainly deteriorate the pulmonary homeostasis maintained by the epithelial IFN subtypes, which is more constitutively expressed by pneumocytes prior to immunopathic IFN responses in severe COVID-19. The gene discussed is IFNA1; the disease is COVID-19.