In an Aβ1–42-induced AD rat model, Exendin-4 engaged PI3K/Akt-signaling to re-invigorate the impaired Akt phosphorylation, mitochondrial function, integrity, respiratory control ratio and ADP phosphorylation, while normalizing mitochondrial complex I, IV, and V activities (which were aberrantly enhanced by the acute Aβ challenge in this study, however) (Garabadu and Verma, 2019). The gene discussed is AKT1; the disease is Alzheimer disease.