Increased activation may cause NF-κB to translocate into the nucleus and subsequently promote the transcription of target gene sequences, including the keratinocyte differentiation markers of cytokeratin 10 (K10), cytokeratin 16 (K16), loricrin (LOR) and filaggrin (FLG) (5–8), and also regulate the cell cycle, which is considered to be significantly accelerated in the pathogenesis of psoriasis (9). Here, NFKB1 is linked to psoriasis.