Based on the clinical and experimental evidence of the strong relationship between inflammation and bone loss, and considering the role played by TNFα, IL-1, and IL-6 in the pathogenesis of changes in bone metabolism in RA, it can be hypothesized that treatments able to inhibit chronic inflammation, and particularly biological agents directed against these cytokines, could potentially inhibit or reverse the different kinds of bone loss observed in this disease. The gene discussed is IL6; the disease is rheumatoid arthritis.