Specifically, the T cell receptor and co-stimulatory molecules (e.g. CD3, CD8)[3, 22, 23]; T cell cytokines (e.g. interferon-γ, IL-13, IL-17, IL-23)[3, 21, 24, 25]; other pro-inflammatory cytokines (e.g. TGF-β, IL-12, IL-18,IL-22)[3, 21, 25–28]; chemokines and receptors (e.g. CXCR1, CXCR2, CXCR3)[3, 21, 29]; adhesion molecules (e.g. ICAM-1, E-selectin, CD18)[21, 30, 31]; and proteases (elastase, cathepsins, and matrix metalloproteinases)[21, 32, 33] have all been implicated in the pathogenesis of psoriasis and COPD. This evidence concerns the gene ICAM1 and psoriasis.