Although the exact mechanism by which B-cells contribute to the cellular and humoral responses that govern MS pathogenesis is still not fully understood, B-cell-targeted therapies have shown promising outcomes in clinical trials3,58 and so if the expression of NgR1 and NgR3 can be therapeutically targeted, then novel pathways for modifying disease specific B-cells may have been identified considering our current data. This evidence concerns the gene RTN4RL1 and myeloid sarcoma.