Chemoresistance is one of the major obstacle for the success of AML treatment.4 One of the main mediators for AML chemoresistance is the multi-drug resistance-1(MDR1) gene and MDR1 protein, also known as permeability-glycoprotein or P-gp.5,6,7 Studies on leukemic blast cells demonstrated the association of MDR1 expression with a lower intracellular retention of cytostatic drugs leading to cancer cell resistance to several commonly used anti-cancer drugs in chemotherapy. Several subsequent studies indicated the influence of MDR1 expression levels in the treatment response and survival of leukemia patients, the frequency of resistance to the chemotherapy increased with increasing MDR1 expression.8,9,10 Previous methods for determination of MDR1 expression have included demonstration of P-glycoprotein by flow cytometry and/or immunohistochemistry, and molecular polymerase chain reaction (PCR)-based assays for RNA expression. However, these assays have either proven difficult to standardize or tedious to perform and they are mainly focused on qualitative or semi-quantitative assays. 11,12 A real-time fluorescence quantitative PCR will increase the sensitivity and also maintain the high specificity. The false positivity caused by pollution of amplification production can also be decreased by hermetization operation. RQ- PCR is a novel methodology which enables sensitive and quantitative measurement of gene expression. 12We have established RQ-PCR method for determination expression of MDR1 gene. We have performed a pilot study with a small cohort of AML patients to determine the relationship of MDR1 expression and CR rate of AML patients. The data shows MDR1 expression has been found in most cases of AML. However, the MDR1 expression levels vary widely from case to case. This result indicated that RQ-PCR method would provide an accurate quantitative measurement for detection of MDR1 expression level in different AML cases who were both positive by qualitative RT-PCR method. 13,14 The pilot results indicated that the complete response rate to induction therapy was compromised by the expression of high levels of MDR1. 15