Chronic Myeloid Leukemia (CML) is a hematological disorder in which the Ph chromosome is a marker of the disease, detected virtually in all cases. The chimeric transcripts encode a 210 kDa chimeric protein with altered tyrosine kinase activity, responsible for eliciting the neoplasic process. The only effective therapy that block the chimeric protein activity is the use of imatinib mesylate (glevec, Norvatis), which binds irreversibly to the BCR-ABL tyrosine kinase blocking the neoplasic activity. Although the extensive utilization of this drug in the clinical therapy of  CML, the proteins and signaling pathways altered during remission of the disease are completely unknown. Furthermore the identification and analysis of the proteomic targets that response to imatinib treatment are extremely necessary to resistant patients follow-up. To address this problem we analyzed through a comparative proteomics approach, the modifications in the protein profile of mononuclear bone marrow cells from patients in imatinib mesylate protocol, that presents hematological and cytogenetic remission, as well as, patients that are non responsive to this drug. The protein extracts, were analyzed through a high-resolution two dimensional (2D) electrophoresis assay with the Multiphor II electrophoresis System (GE). Seven hundred micrograms of each sample was precipitated and used in the 2-D gels. The proteins were separated using a 11cm ImmobilineDrystrip (GE) of pH 4-7, for 78kVh. The second dimension was done in a 8-18% gradient SDS-PAGE gel in a Multiphor II (GE) apparatus. The gels were analyzed and all protein-spots were identified by Mass spectrometry in a MALDI-TOF-TOF instrument (4700 Applied Biosystems). Using this approach we identified 200 proteins present in all samples and 13 differentially expressed protein spots between the samples. These results show that the proteomic pattern of patients that respond to treatment seams to be likely to the protein profile of the chronic and blastic phase except by one of the protein that could represent a phosphorylated biomarker, NuMA1 protein, a BCR-ABL target.