The findings that TNFR2 is highly expressed in microglia/macrophages in the MS WM both before and during active demyelination and that TNFR2 can be activated by an exogenous compound to promote endogenous myelin formation in an ex-vivo experimental model has translational relevance for MS therapy and may stimulate the development of drugs specifically targeting TNFR2. Here, TNFRSF1B is linked to myeloid sarcoma.