Abstract
Imatinib is approved as the first-line treatment for newly diagnosed chronic myelogenous leukemia (CML). In spite of profound response in the majority of patients, resistance occurs in a subgroup of CML cases. Recently, it has been demonstrated that different classes of non-coding RNAs can modulate response to this tyrosine kinase inhibitor. Recognition of the role of these transcripts in this process not only expands our knowledge about the molecular mechanisms of imatinib resistance, but also provides novel strategies for combating this phenotype. The current review summarizes the role of non-coding RNAs in this process and suggests novel candidates for further studies in this field to enhance therapeutic response to imatinib.