This review will discuss how insufficient immune control might allow for sizeable populations of T-bet<sup>+</sup>CXCR3<sup>+</sup> B cells to infiltrate the central nervous system (CNS), attract other lymphocytes, efficiently stimulate T cells in the CNS, and differentiate into antibody-producing plasma cells, thereby contributing to inflammation and autoantibody production in a subset of MS patients. This evidence concerns the gene CXCR3 and myeloid sarcoma.