Sustained activation of synovial effector cells in the RA joint is created by secretion of interleukin (IL)-1β and tumour-necrosis factor (TNF) by macrophages, triggering release of granulocyte–macrophage colony-stimulating factor (GM-CSF) and IL-6 from FLS which in turn activates macrophages [7, 8]. The gene discussed is TNF; the disease is rheumatoid arthritis.