Although IFN-γ is primarily thought to be pathogenic in the context of MS, the deletion of the cytokine or the receptor in transgenic knockout (KO) mice exacerbates EAE clinical symptoms and results in the accumulation of autoreactive CD4+ T cells in the CNS, demonstrating that IFN-γ is necessary to limit autoimmunity by inhibiting T-cell proliferation and inducing the apoptosis of activated CD4+ T cells.246 Some years later, Th17 cells were identified as a novel Th subtype of pathogenic cells whose differentiation and expansion are dependent on IL-23. This evidence concerns the gene CD4 and myeloid sarcoma.