We reproduced this potentially reversible response by human adult mature OLs in both dissociated cell culture and microfibre ensheathment assays, using an array of insults implicated in MS pathogenesis including the pro-inflammatory molecules interferon (IFN)-γ and tumor necrosis factor (TNF)-α, the excitatory neutrotransmitter glutamate, and metabolic stress conditions involving nutrient deprivation and low glucose19,42. This evidence concerns the gene TNF and myeloid sarcoma.