However, all animal models of psoriasis carry inherent limitations and although keratinocyte signal transduction after stimulation with TPA or imiquimod shows similarities, e.g., with involvement of nuclear factor kappa B (NF-kB) and signal transducer and activator of transcription 3 (STAT3) pathways, important differences between imiquimod-induced skin inflammation and psoriatic plaques were recently demonstrated [36, 37]. Here, NFKB1 is linked to psoriasis.