Given the involvement of Willin/FRMD6 in cellular functions such as ERK signaling and cytoskeletal organization that are critical in the maintenance of mitochondrial homeostasis and the role of mitochondrial dysfunction in early AD pathogenesis, we hypothesize that oxidative stress and alterations in mitochondrial function represent a mechanism linking Willin/FRMD6 to AD pathogenesis. Here, FRMD6 is linked to Alzheimer disease.