Therefore, the production, aggregation, and clearance of Aβ were considered to be related to the pathogenesis of AD, and multiple strategies have been tried to treat AD by (i) inhibiting β- and γ-secretases which are responsible for the generation of Aβ by cleaving amyloid precursor protein (APP) [10, 11], (ii) modulating Aβ aggregation [2], and (iii) enhancing the removal of Aβ [12–15]. The gene discussed is PPIB; the disease is Alzheimer disease.