The pathophysiological significance of this response is unclear as FGF2 is functionally pleiotropic, experimental studies demonstrating that in addition to its detrimental effects on remyelination it also supports OPC proliferation and migration [2, 9, 11], as well as mediating a neuroprotective response which reduces clinical deficits and tissue damage in animal models of MS [66, 68]. Here, FGF2 is linked to myeloid sarcoma.