In agreement with theseexperimental data, patients with severe inflammatory disease have significantlyhigher serum resistin concentrations, while patients with rheumatoid arthritis(RA) show increased resistin levels in their inflamed joints that correlatewith markers of inflammation [11].Furthermore, PPARγ agonists and HMG-CoA reductase inhibitors (statins), both recognized fortheir anti-inflammatory properties, decrease macrophage resistin mRNA andprotein secretion, apparently via the NF-κB pathway [12, 13]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.