γ-Secretase, which is one of the top targets for developing AD therapeutics with disease-modifying effects, cleaves the transmembrane region of APP to produce Aβ of variable length [10-12], with Aβ1-40 being the most abundant isoform, whereas Aβ1-42 is most prone to aggregation [13,14]. The gene discussed is APP; the disease is Alzheimer disease.