Reduction of BCR-ABL1 mutant clones after discontinuation of TKI therapy

In this letter we describe two case reports of CML patients with acquired mutations of the BCR-ABL1 kinase domain, in whom the mutant clone regressed and drug sensitivity was restored after temporary interruption of TKI. We believe that temporary interruption of an ATP-competitive tyrosine kinase inhibitor and switching to non-selective therapy can be a valid therapeutic option in CML patients. In addition, we highlight the potential of a flow cytometric CRKL phosphorylation assay to explore TKI sensitivity in CML cells ex vivo, and its correlation with clinical and haematological sensitivity or resistance.