In the past 15 years, several phase II/III clinical trials with antagonists against the chemokine receptors CCR1, CCR2, CCR3, CCR5, CCR9, CXCR1, CXCR2, and CXCR3 have failed to have significant clinical benefits in patients with autoimmune and inflammatory diseases, such as RA, multiple sclerosis (MS), IBD, psoriasis, and asthma (4, 5). The gene discussed is CCR2; the disease is rheumatoid arthritis.