In psoriasis mouse models, deletion of S100A9 improves psoriasis-like skin disease, and studies on adenovirus induced overexpression of S100A8/A9 in human keratinocytes show increased levels of TNF-alpha, IL-6 and IL-8 in cell medium suggesting a pro-inflammatory effect and important role for S100A8/A9 in psoriasis pathogenesis [13, 14]. Here, CXCL8 is linked to psoriasis.