Indeed, several inborn defects of IFN immunity have been found in critical (especially younger) COVID-19 patients: autosomal recessive deficiencies of IFNAR1 and IRF7 (1.8% of cases), X-linked deficiency of TLR7 (1.3%), newly described or known autosomal dominant deficiencies of IFNAR1, IFNAR2, TLR3, IRF3, TRF, TBK1, UNC93B1 (2.9%), enhancing the risk of a severe disease course 20 to 34-fold (68–70). The gene discussed is IFNAR1; the disease is COVID-19.