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. The gene discussed is TP53; the disease is psoriasis.