Accordingly, LY3009120, navitoclax, imatinib, and quizartinib combine significantly with hydroxyurea against leukemic cells with BCR-ABL1 and FLT3-ITD, and these drugs break the resistance of CML cells to hydroxyurea-induced apoptosis. The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.