Chronic myeloid leukemia (CML) is a stem cell disease which is typical for increased and unregulated accumulation of predominantly clonal myeloid cells in hematopoietic tissue. Specific translocation t(9;22) that creates the BCR/ABL on chromosome which are known as the 'Philadelphia chromosome ' can be detectable in CML patient. The most effective curative approach available to date so far is stem cell transplantation. BCR/ABL tyrosine kinase inhibitor (Imatinib) interferonalpha (with or without ARAC), or other Immunotherapy are other options for those who cannot get stem cell transplantation. Tyrosine kinase inhibitors (TKIs) have dual mode of actions: direct oncokinase inhibition and restoration of effectorm ediated immune surveillance. These mechanism of actions induce the high rate deep molecular response in CML patients. CCyR( complete cytogenetic response) or MMR(major molecular responses) are primary goals for the initial therapy. However mutation on BCR/ABL provoked resistance over imatinib therapy and further studies has shown that the early monitoring of responses during the treatment has a crucial role for assessing TKIs therapy. Thus it is important to continue research on therapies that increases durable complete molecular responses and this can be achieved with further generations of TKIs or combination with other available agents.