We then examined whether inhibition of Akt function in Akt-expressing ovarian cancer cells (A2780cp) with dominant negative Akt adenovirus (Adv–DN-Akt—a dead kinase mutated at three phosphorylation sites: K179A, T308A, and S473A) and p53–Adv reconstitution together would detach mito-HKII from the OMM and elicit chemosensitivity. The gene discussed is TP53; the disease is ovarian carcinoma.