The search for the encephalitogenic factor driving pathogenic T cells in autoimmune diseases such as rheumatoid arthritis, multiple sclerosis (MS), and psoriasis has proven to be a long and difficult mission, which is not yet completed. In this issue of the European Journal of Immunology, the importance of the transcription factor T‐bet, previously shown to be essential for the induction of autoimmune disease in mice, is challenged. Two independent groups, O'Connor et al. [Eur. J. Immunol. 2013. 43:2818–2823] report] and Grifka‐Walk et al. [Eur. J. Immunol. 2013. 43:2824–2831], report that T‐bet is not mandatory for T cells to cause experimental autoimmune encephalomyelitis (EAE), which serves as a paradigmatic T‐cell‐mediated autoimmune disease. Both groups found that T‐bet KO mice were fully susceptible to develop EAE, both after immunization with self‐antigen and after adoptive transfer of IL‐23‐polarized autoaggressive T cells. T‐bet deficiency mediated the loss of IFN‐γ expression but retained or even enhanced GM‐CSF and IL‐17 production by central nervous system (CNS)‐infiltrating T cells. These findings indicate that we have lost the last transcriptional regulator previously held to be required for the generation of autoimmune pathogenic T cells.