This view is further supported by the work of Leuner and colleagues [45], which, by means of in vitro and in vivo models of AD, showed that mitochondria-derived ROS are able to trigger the amyloidogenic amyloid precursor protein (APP) processing, leading to Aβ formation, thus demonstrating the strong influence that mitochondria and Aβ can have on each other [46]. The gene discussed is APP; the disease is Alzheimer disease.