Thus, DMF activation of NRF2 through two distinct proteolytic pathways, a KEAP1 dependent one and the other mediated by GSK-3β phosphorylation (Figure 2), makes this compound a promising therapy for neurodegenerative diseases as tauopathies, where either KEAP1 or GSK-3β activities are altered [14]. This evidence concerns the gene GSK3B and neurodegenerative disease.