Using the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis, which recapitulates CD4+ T cell-dependent disease, Itoh, et al. [157] showed that KDM6A deletion in CD4+ T cells ameliorated clinical disease, reduced neuropathology and downregulated the expression of neuroinflammation pathway genes, also providing an X dosage-dependent mechanism for sex differences in autoimmune diseases affecting the nervous system. The gene discussed is CD4; the disease is multiple sclerosis.