As the central molecule in the immune microenvironment of psoriasis, IL-17A/IL17A, IL-17F/IL-17F homodimers, and IL-17A/IL-17F heterodimers mediate the ligation in initial subcellular events of IL-17RA/RC and downstream signals by recruiting and activating ACT1, TRAF6, and CARD14 complexes.180 TRAF6 further activates the NF-κB pathway by activating IKK, consequently leading to proteasomal degradation of phosphorylated IκB. Here, NFKB1 is linked to psoriasis.