In the last two decades, our knowledge of the immunopathogenic mechanisms of MS has strongly improved, thus evidencing a fundamental role of encephalitogenic Th cells, in particular, Th1-Th17 like, Th17, Th22, and GM-CSF-producing CD4+ T cells, in initiating and perpetuating the inflammatory responses and the consequent neurodegeneration in MS. The gene discussed is CSF2; the disease is myeloid sarcoma.