Consistent with this, the metabolic injury to oligodendrocytes that were experimentally induced via intoxication with cuprizone [38] is increased in Nrf2−/− compared to wild-type mice [39], while the activation of NRF2, especially in GFAP+ astrocytes, improved the pathology in a toxin-induced demyelination model [40]. Here, NFE2L2 is linked to Peripheral demyelination.