Although the pathophysiological mechanisms of MS remain largely unknown, studies have implicated autoreactive T cells (primarily, T helper (Th)-1 CD4+ T cells and Th17 cells) as being involved, particularly through their secretion of cytokines and activation of the inflammatory cascade; the eventual result is demyelinating plaques—the pathological hallmark of MS. This evidence concerns the gene CD4 and myeloid sarcoma.