Over the past decade, tyrosine kinase inhibitor (TKI) therapy has transformed chronic myeloid leukaemia (CML), caused by the BCR‐ABL fusion‐oncoprotein,1 from a fatal disease into a chronic ailment.2 Actually, survival of CML patients is mainly determined by comorbidities rather than by the disease itself.1, 3, 4 Hence, for CML patients with optimal response to TKIs and long‐term survival, treatment‐free remission (TFR) has become a therapeutic goal. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.