Their role in the pathogenesis of critical COVID-19 was discovered after a few patients were found to suffer from critical COVID-19 because of IEI of type I IFN immunity, including previously healthy adults with autosomal recessive IFNAR1 or IRF7 deficiency (83), or because of autoimmune polyendocrinopathy syndrome type I (APS-1), a condition underlying the development of multiple auto-Abs, including auto-Abs neutralizing type I IFNs, due to AIRE mutations impairing the deletion of autoreactive T cells in the thymus (84, 85). The gene discussed is IRF7; the disease is COVID-19.