The results demonstrated that the overexpression of REST greatly repressed the release of cytochrome c (16.2% of the negative control), which acts downstream in the mitochondrial apoptotic pathway, and enhanced the expression of the anti-apoptotic protein, transcription factor FOXO1 (by 2.6 fold relative to the negative control), which mediates oxidative stress resistance [46] [47] and is protected by REST in AD [16]. The gene discussed is FOXO1; the disease is Alzheimer disease.