Chronic myeloid leukemia (CML) is characterized by the production of BCR-ABL oncoprotein that has enhanced tyrosine kinase activity. The use of imatinib has redefined the survival of CML patients. Further understanding of disease pathogenesis has led to the identification of quiescent CML Leukemic Stem Cells (LSC) that are resistant to tyrosine kinase inhibitors (TKI) and lead to failure to achieve complete molecular response in many patients. The PPAR-γ agonists can purge them out of quiescence, thereby sensitizing them to imatinib. Hence, combining the two can act in synergy to deplete the leukemic cells. The objective of our study was to determine if the addition of PPAR-γ agonist, pioglitazone to imatinib could attain major molecular response (MMR) in patients who fail to achieve optimal response with imatinib.