The present study demonstrated that the combination of a human PARP inhibitor (olaparib) and an Akt inhibitor (capivasertib) significantly impaired mitochondrial oxidative phosphorylation in both (MCF7) and (MDA-MB-231) breast cancer cell lines without inducing compensatory glycolytic activation (Figure 6), thereby generating a considerable reduction in overall ATP production in both cell lines (Figure 5c,d). The gene discussed is PARP1; the disease is breast cancer.