Cytokine-mediated regulation of NKG2D in CD4+ T cells has not yet been fully understood, but, at least, there is also evidence concerning the influence of pro-inflammatory cytokines on NKG2D induction; one example is a report showing that a substantial number of peripheral and synovial CD4+CD28− T cells in patients with rheumatoid arthritis expressed NKG2D under the influence of IL-15 and TNF-α, which endowed this T cell population with cytotoxic activity and the ability to lyse synoviocytes aberrantly expressing NKG2D ligands [21]. The gene discussed is CD28; the disease is rheumatoid arthritis.