In particular, the resistance might be ascribed to four major events: i) gene amplification or mutations at the kinase site; ii) decreased intracellular IM levels due to enhanced activity of drug exporters and activation of alternative pathways functionally compensating for IM-sensitive mechanisms; iii) induction of immature CML cell quiescence, and iv) suppression of BCR-Abl1 expression [16–21]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.