As an example, in COVID-19, endogenous high levels of type I IFN are protective (50) and early administration of IFN-α decreases mortality, while late administration of IFN-α increases mortality (51); this is consistent with the fact that delayed or chronic IFN responses disrupt lung repair and induce immunopathology (52, 53), while early administration of type I IFN is protective in IFV and coronavirus infections (49, 53). The gene discussed is IFNA1; the disease is COVID-19.