Although T-bet was shown to be required for the generation of Th1-like Th17 cells or Th1-like exTh17 cells in several autoimmune disease settings, adoptive transfer of T-bet-deficient Th17 cells induced attenuated or comparable disease compared to transfer of WT Th17 cells depending on the experimental model34–39. Here, TBX21 is linked to autoimmune disease.