In line with these findings, others have shown that RA SF contains significantly higher levels of CXCL10 compared to SF from patients with OA or traumatic joint injury [5] and that deletion of either CXCL10 or its receptor CXCR3 significantly abrogates CD4+ T cell infiltration in murine arthritis models [22]. The gene discussed is CXCR3; the disease is rheumatoid arthritis.