On the effector side, T cells from the inflamed joints are resistant to Treg cell-mediated suppression thanks to protein kinase B (PKB) hyperactivation in JIA.9, 10 In addition, we recently described a subset of circulating antigen-experienced, proinflammatory effector T (Teff) cells that are resistant to anti-tumor necrosis factor (TNF) therapy and are enriched in synovial clonotypes.11 Teff resistance to Treg cell-mediated suppression is also recognised in RA.12 The gene discussed is TNF; the disease is rheumatoid arthritis.