Multiple toll-like receptor (TLR) and immune-related signaling pathways were significantly enriched in our gene list, such as signaling by interleukins and NF-κB activation, characterizing the inflammatory cascade observed during the psoriasis pathogenesis, while cellular, mitotic-associated processes including the transcriptional regulation by TP53, cellular senescence and keratinization further validated the aberrant hyperproliferation of keratinocytes in the cutaneous inflammation. This evidence concerns the gene NFKB1 and psoriasis.