The reduction in phosphorylated FOXO3a content in the hippocampus in 13‐month‐old APP/PS1 mice likely represents decompensatory alterations in the amyloidogenic pathway in the late stage of AD, whereby the entry of nonphosphorylated FOXO3a into the nucleus induces cell cycle arrest and apoptosis, resulting in the formation of numerous Aβ plaques and late neuronal apoptosis. The gene discussed is APP; the disease is Alzheimer disease.