Accordingly, the critical role of CCR2/CCL2 in various inflammatory pathogeneses, including rheumatoid arthritis (Bayley et al. 2003; Quinones et al. 2004), asthma (Blease et al. 2000; Rose et al. 2003), multiple sclerosis (Izikson et al. 2000; Fife et al. 2000; Huang et al. 2001), neuropathic pain (Abbadie et al. 2003), or atherosclerosis (Boring et al. 1998), has been largely documented and demonstrated in mice that are deficient for CCL2 or CCR2. This evidence concerns the gene CCL2 and rheumatoid arthritis.