Inappropriately normal plasma cortisol and a blunted response of plasma cortisol to surgical stress have been shown for RA patients.1,2 Glucocorticoids (Gcs) are required for the development of streptococcal cell wall-induced arthritis in Lewis rats.3 Furthermore, while many RA patients respond well to exogenous Gc treatment, a proportion fail to do so.4 These observations suggest that hypothalamic-pituitary-adrenal (HPA) axis dysregulation or relative Gc deficiency contributes to the onset of RA. This evidence concerns the gene GC and rheumatoid arthritis.