Genetic and environmental factors are thought to contribute to either the initial susceptibility to synovitis or persistence of joint disease in patients with rheumatoid arthritis. The genetic component of the disease probably accounts for no more than 12–15% of the whole, only one-third to one-half of this component can be accounted for by genes encoded within the HLA complex which may influence disease severity rather than susceptibility (1). At present the recognition of specific HLA markers for more aggressive forms of the disease has not yet been translated into any form of successful therapy. Further, therapies aimed at CD4⁺ T-cells have not been successful, as also predicted from lack of amelioration of arthritis in AIDS patients. Clearly other risk factors need to be established in order for new therapeutic strategies to be developed.