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However, our in vitro data suggest that apoptosis induction after transient TKI treatment, observed in the BCR\u2013ABL\u2010positive cell lines K562, KYO\u20101, and LAMA\u201084 and progenitor cells from chronic phase CML patients, is instead caused by a residual kinase inhibition that persists in the cells as a consequence of intracellular drug retention. High intracellular concentrations of imatinib and dasatinib residues were measured in transiently treated cells. Furthermore, the apoptosis induced by residual imatinib or dasatinib from transient treatment could be rescued by washing out the intracellularly retained drugs. The residual kinase inhibition was also undetectable by the phospho\u2010CRKL assay. These findings confirm that continuous target inhibition is required for the optimal efficacy of kinase inhibitors. Am. J. 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