The introduction of imatinib, the tyrosine kinase inhibitor (TKI), in the early 21st century is considered a breakthrough in the treatment of CML. In the vast majority of patients, treatment with imatinib induces cytogenetic and even molecular responses with very low or undetectable BCR-ABL1 transcript levels. These patients remain free from progression to blast crisis. However, imatinib does not cure the disease because it is unable to eradicate the leukaemic stem cells, which therefore provides a potential reservoir for relapse.