Finally, as a result of the impaired homology-mediated DNA repair, we observed a substantial decrease of viability in AKT-inhibited tumor cells after Dox treatment, which was evidenced by MTS-based colorimetric assay and increased expression of apoptotic markers (cleaved forms of caspase-3 and poly-(ADP)-ribose-polymerase (PARP) and the numbers of hypodiploid cells). The gene discussed is AKT1; the disease is neoplasm.