The study investigates the role of TGF-β signaling in the differentiation of pathogenic Th17 cells. It demonstrates that Th17 differentiation can occur in the absence of TGF-β signaling, as evidenced by the induction of IL-17 production by IL-6, IL-1β, and IL-23 in the absence of TGF-β. The epigenetic modification of the *Il17a*/*Il17f* and *Rorc* promoters is also observed without TGF-β, allowing the generation of Rorγt+ T-bet+ Th17 cells. These cells are found in the CNS during experimental allergic encephalomyelitis (EAE) and adoptively transferred into EAE mice, showing enhanced pathogenicity compared to conventional Th17 cells. The study highlights the importance of IL-23 and T-bet in the development of pathogenic Th17 cells, suggesting potential therapeutic targets for autoimmune diseases.The study investigates the role of TGF-β signaling in the differentiation of pathogenic Th17 cells. It demonstrates that Th17 differentiation can occur in the absence of TGF-β signaling, as evidenced by the induction of IL-17 production by IL-6, IL-1β, and IL-23 in the absence of TGF-β. The epigenetic modification of the *Il17a*/*Il17f* and *Rorc* promoters is also observed without TGF-β, allowing the generation of Rorγt+ T-bet+ Th17 cells. These cells are found in the CNS during experimental allergic encephalomyelitis (EAE) and adoptively transferred into EAE mice, showing enhanced pathogenicity compared to conventional Th17 cells. The study highlights the importance of IL-23 and T-bet in the development of pathogenic Th17 cells, suggesting potential therapeutic targets for autoimmune diseases.