In the current contribution, imatinib plus 10 μM of ketoconazole was applied to resistant (K562-RI) CML cells with the aim of decreasing the overexpression of P-gp, enhancing the intracellular concentrations of imatinib, and accelerating the rate of programmed cell death. The gene discussed is PGP; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.