Given that anti-TNF and anti-IL-6 therapies have been successful in RA and that head-to-head trials between anti-GM-CSFRα and anti-TNF are ongoing [2], it would be useful to know how similar or not the biology of the pro-inflammatory activity of GM-CSF is to the respective biology of these other cytokines. The gene discussed is CSF2; the disease is rheumatoid arthritis.