CXCL8 and psoriasis: Li et al. reported that NF-κB acts as a key bridge which links the activated Th1 cells with the transcription of many crucial genes involved in the pathogenesis of psoriasis, such as TNF-α, IL-8, IL-12, and cyclin D, and suggested that the dysfunction of NF-κB may contribute to the formation or aggravation of psoriasis [11].