In contrast, the gene encoding the sMAF protein MafF is markedly increased in AD, which may partly explain the defect in Nrf2 stimulation (Wang et al. 2017): increased MarF promotes its homodimer formation, leading to repression of Nrf2 (Igarashi et al. 1994) (Fig. 3d). This evidence concerns the gene NFE2L2 and Alzheimer disease.