Typical pathological features of AD include the deposition of β-amyloid plaques due to the accumulation of amyloid-beta oligomers (AβO) [1], which is generated by the sequential proteolytic cleavage of transmembrane amyloid precursor protein (APP) by β-secretases and γ-secretases, which are considered critical initiators of AD [2,3]. The gene discussed is APP; the disease is Alzheimer disease.