Psoriasis is considered to primarily be a T cell-mediated immune disease, and Th1 and Th17 lymphocytes are expected to be the main players via the release of inflammatory cytokines (i.e., IL-1α, IL-1β, IL-17, IL-22, TNF-α), leading to keratinocyte proliferation, the migration of inflammatory cells, and enhanced inflammatory response in the skin [15,16,17]. This evidence concerns the gene IL17A and psoriasis.