Interestingly, in nontransformed colonocytes, inflammatory cytokines (e.g., TNF-α) could induce strong ERBB4 expression through a mechanism involving NF-κB signaling [42], while both TNF-α and NF-κB play crucial roles in psoriasis pathogenesis [34, 43–45]. This evidence concerns the gene NFKB1 and psoriasis.