LAUSR

has displayed better efficacy than imatinib in achieving MMR 4 hronic myeloid leukemia (CML) has become a model of sucess in the history of hematology. That is due to the possibility f discovering and monitoring the molecular basis of the disase and blocking it by employing tyrosine kinase inhibitors TKIs).1 In the beginning of the XXI century, chemotherapy nd the recombinant interferon-alpha were overcome by the fficiency of the TKIs in chronic-phase (CP) CML patients. pproximately 80% of the patients presenting CP-CML treated ith imatinib achieved complete cytogenetic remission (CCR). oreover, these patients also present extraordinary long surival rates. Firstly, imatinib demonstrated that a fatal cancer ould become a chronic comorbidity. Soon after the first eneration of TKIs, owing to the development of imatinibesistance, other TKIs were developed, such as: dasatinib, ilotinib, bosutinib and ponatinib.