To test whether this mechanism is also operative in an independent BCR-ABL driven cell model and in primary human cells, we then investigated imatinib release upon HD-TKI pulse-exposure using different cell populations: Ba/F3-BCR-ABL cells as well as mononuclear cells from untreated CML patients and normal CD34+ hematopoietic progenitor cells from healthy donors exhibited the same kinetics as previously demonstrated for K562 cells (Figure 7A, panels II–IV). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.