In rheumatoid arthritis, individuals with active rheumatoid arthritis have increased expression of NLRP3 and NLRP3‐mediated interleukin‐1β secretion in whole blood cells.81 In experimental arthritis, deletion of Nlrp3, caspase‐1 and the interleukin‐1 receptor markedly protects against rheumatoid arthritis‐associated inflammation and cartilage destruction.82 Together, the data strongly indicate that NLRP3 inflammasome deregulation is implicated in the pathogenesis of atherosclerosis, diabetes mellitus type 2 and obesity and, to a lesser extent, rheumatoid arthritis. The gene discussed is NLRP3; the disease is arthritic joint disease.