Multiple sclerosis (MS), an inflammatory demyelinating disease affecting the central nervous system (CNS), has multiple clinical manifestations including vision loss, exercise, sensory impairment, or disability.1 It is generally believed that MS is caused by peripherally activated autoreactive effector factor CD4+ T cells that cross the blood–brain barrier (BBB) into the CNS, where they are re-activated by antigen-presenting cells (APCs) and secrete inflammatory cytokines (e.g., IFN-γ, TNFα, IL-17, GM-CSF, and IL-22). This evidence concerns the gene IL17A and myeloid sarcoma.