Experiments investigating the mechanisms responsible for cognitive deficits in MS, showed impairment in the induction of hippocampal long-term potentiation (LTP, the electrophysiological correlate of memory formation functions) associated with an altered NMDAR homeostasis, an increase in the hippocampal microglial infiltration and high levels of IL-1β [99]. Here, IL1B is linked to myeloid sarcoma.