Current therapies interfere with the activity of key proinflammatory cytokines (e.g., tumor necrosis factor [TNF] inhibitors in inflammatory bowel disease [IBD], and TNF and interleukin [IL]-6 inhibitors in rheumatoid arthritis) or target specific immune cells (e.g., B-cell modulation by belimumab in systemic lupus erythematosus [SLE]) (1, 2). The gene discussed is TNF; the disease is rheumatoid arthritis.