While counterintuitive, given that progressive mitochondrial dysfunction is well characterized in AD patients and APP/PS1 mice, mild MCI inhibition in dysfunctional mitochondria could decrease ROS production, while in functional mitochondria could improve energetics, as we demonstrated previously69, and through activation of stress responses, could promote biogenesis and mitophagy, contributing to a healthier mitochondrial pool and more effective energy production. The gene discussed is APP; the disease is Alzheimer disease.