TCRαβ+DNT, as a minor portion of αβ T cells that lack CD4 and CD8 markers, has been considered to contribute to many autoimmune diseases, such as autoimmune lymphoproliferative syndrome (ALPS), systemic Lupus Erythematosus (SLE), and psoriasis, along with their ability to help B cells produce autoantibodies and various pro-inflammatory cytokines including IL-17, IFN-γ, and IL-4 (11, 18, 19). This evidence concerns the gene CD4 and psoriasis.