Imatinib mesylate, binding to the inactive conformation of Bcr-Abl tyrosine 
kinase and suppressing the Ph chromosome positive clone, has revolutionized the 
treatment of chronic myeloid leukaemia (CML) patients. Given the high rates of 
clinical and cytogenetic remission achieved, the molecular monitoring of BCR-ABL 
transcript levels by RT-qPCR has become always more important to assess minimal 
residual disease. Recently, recommendations for harmonizing current 
methodologies for detecting and measuring BCR-ABL transcripts in CML patients 
have been suggested. Studies of imatinib-treated patients have determined that 
the BCR-ABL levels measured early in therapy may predict durable cytogenetic 
remission and in turn prolonged progression free-survival or acquisition of 
resistance. The major mechanism of imatinib resistance is clonal expansion of 
leukaemia cells with mutations in the Bcr-Abl fusion tyrosine kinase. The early 
reduction of such mutations may allow timely treatment intervention to prevent 
or overcome resistance. We review current trends in the management of chronic 
myeloid leukaemia patients undergoing treatment with tyrosine kinase inhibitors.