NFE2L2 and Alzheimer disease: Supporting the notion that NRF2 is needed to prevent Aβ-driven AD pathogenesis, mice genetically engineered to overexpress NRF2 in an AD context (Keap1FA/FA;APPNLGF) exhibited increased glutathione, decreased oxidative stress and inflammation, and improved cognition compared to wildtype, with similar benefits being obtained via administration of the isothiocyanate 6-(Methylsulfinyl)hexyl isothiocyanate (6-MSITC) (Uruno et al., 2020).