The pathogenesis of RA is suggested to involve Th1-type T cells that preferentially express CCR5 where its chemokines ligands (macrophage inflammatory protein (Mip)-1α, CCL3; and Mip-1β, CCL4) participate in selective recruitment of CCR5 + CXCR3+ T cells to the inflamed synovium [27]. The gene discussed is CXCR3; the disease is rheumatoid arthritis.