We have demonstrated that loss of Nr2f6 exacerbates experimental autoimmune encephalomyelitis (EAE); mechanistically, NR2F6 serves as a negative regulator of Il17 expression through DNA binding and competition for NFAT/AP‐1 transcription factor binding sites, thus reducing IL‐17 expression and pathogenesis of Th17 cells [220]. The gene discussed is NR2F6; the disease is experimental autoimmune encephalomyelitis.