In arthritis and periodontitis, cytokines, such as interleukin (IL)-17, tumor necrosis factor (TNF), IL-6, and IL-1β, produced by diverse cells of innate and adaptive immunity, contribute to synovial or gingival inflammation and amplify bone erosion via direct or indirect stimulation of osteoclast generation and activation, in part by upregulating expression of RANKL in different cell types, including synovial fibroblasts in arthritis.2,19–23. The gene discussed is TNFSF11; the disease is arthritic joint disease.