In stark contrast, using experimental autoimmune encephalomyelitis, we show that IL-17ACre–mediated deletion of Tbx21 prevents the conversion of Th17 cells to IL-17A/IFN-γ double-producing cells as well as Th1-like IFN-γ+ ex-Th17 cells. Here, TBX21 is linked to experimental autoimmune encephalomyelitis.