Therefore, the costimulatory signal triggered by the engagement NKG2D/NKG2D ligands coupled with suboptimal stimulation via TCR will induce important cytokine and cytotoxic responses, thereby self-perpetuating the CD4+NKG2D+ T cell autoreactivity in rheumatoid arthritis[40,41]. The gene discussed is KLRK1; the disease is rheumatoid arthritis.