In genetically predisposed individuals, the virus infection triggers the activation of TLR‐7/8 and/or RIG‐I antiviral signaling and subsequently induces IL‐23 expression in the CD11c+ DCs via the NF‐κB pathway, and genetic mutations in genes such as TNFAIP3, TNIP1, NFKBIA, TRAF3IP2, and CARD14 result in an impaired negative regulation of NF‐κB proinflammatory activity (Nair et al, 2009; Genetic Analysis of Psoriasis et al, 2010; Huffmeier et al, 2010; Jordan et al, 2012), thereby leading to psoriasis (Fig EV5). This evidence concerns the gene NFKB1 and psoriasis.