As in RA patients the synovial joint (tissue and SF) contains several ligands for both CCR2 and CCR5 [1], [8]–[13] that are responsible for monocyte recruitment to these compartments (via many receptors such as CCR1 [21]), this redundancy could have accounted for the observed chemokine receptor blockade failure in both our in vitro model and in the clinical trials. The gene discussed is CCR1; the disease is rheumatoid arthritis.