Like ALS, NRF2 was shown to be upregulated in MS patient lesions (Licht-Mayer et al., 2015), and transgenic activation of NRF2 specifically in astrocytes prevented, whereas whole body knockout exacerbated, the oligodendrocyte loss and enhanced inflammation observed in a cuprizone-induced model of MS (Draheim et al., 2016; Nellessen et al., 2020). Here, NFE2L2 is linked to amyotrophic lateral sclerosis.