Antibody-dependent mechanisms promote MS pathogenesis by producing autoantibodies against specific CNS tissues, while antibody-independent mechanisms promote MS pathogenesis by inducing B-cell receptor (BCR) internalization of autoantigens and presentation to specific CNS pathogenic T cells to promote T-cell activation, by producing cytokines and by forming ectopic lymphoid tissue (11). This evidence concerns the gene BCR and myeloid sarcoma.