Of note, the cells possessing a substantial amounts of p-AMPK, p-mTOR and p-tau displayed a significant reduction of PRDX1 and PRDX4 along with an increased level of mitochondrial DNA and cellular protein oxidation, suggesting that downregulation of antioxidant enzymes and oxidative stress are the early events triggering AMPK/mTOR activation in AD [36]. The gene discussed is PRDX1; the disease is Alzheimer disease.