Dimethyl fumarate disrupts the interaction between Keap1 and Nfr2 by alkylating cysteine residues in Keap1, which results in Nrf2 translocation to the nucleus and activation of mitochondrial biogenesis in multiple sclerosis (Hayashi et al., 2017) and MPTP-induced model of Parkinson’s disease (Ahuja et al., 2016). This evidence concerns the gene KEAP1 and multiple sclerosis.