However, it has been reported, in an animal model of RA, that the administration of an anti-CXCR3 MoAb (a chemokine receptor that is expressed by different immune cells, including Th17 lymphocytes) significantly reduces the inflammation and articular damage, with diminution of proinflammatory mediators (e.g., TNF-α, interferon-γ (IFN-γ), IL-17A, and IL-22) and increased levels of Foxp3+ T regulatory (Treg) cells [2]. The gene discussed is IL17A; the disease is rheumatoid arthritis.