Synovial fibroblasts have been identified as a significant source of GM-CSF.31 We assessed their contribution by stimulating cultured synovial fibroblasts with IL-1β and TNFα, two cytokines produced by synovial macrophages and thought to be responsible for the activated phenotype of RA synovial fibroblasts.32 Whereas levels of GM-CSF were undetectable following stimulation with up to 50 ng/mL TNFα (data not shown), IL-1β was an effective stimulus for GM-CSF production (figure 1B). The gene discussed is TNF; the disease is rheumatoid arthritis.