Using overexpression systems, 24 variants (including the pLOF ones) in TLR3, UNC93B1, IRF7, IRF3, TICAM1/TRIF, TBK1, IFNAR1, IFNAR2 were demonstrated to be deleterious, since they were loss-of-expression, LOF or severely hypomorphic; of these 24 variants, four were autosomal-recessive (AR) deficiencies (homozygosity or compound heterozygosity for IRF7; homozygosity for IFNAR1) and 19 AD deficiencies (TLR3, TICAM1, TBK1, IRF3, UNC93B1, IRF7, IFNAR1, and IFNAR2). Here, IFNAR2 is linked to Alzheimer disease.