In committed CP-CML cells, the BCL2 and BCR-ABL1 kinase dual targeting demonstrated superior antileukemic activity, compared to either inhibition alone, suggesting that more differentiated leukemic cells are dependent on BCL2 and BCR-ABL1 kinase cooperation for their survival. This evidence concerns the gene BCL2 and chronic myelogenous leukemia, BCR-ABL1 positive.