The aim of this study was to map the transcriptional response of cells to the activity of the fusion oncogene BCR/ABL1, associated with chronic myeloid leukemia (CML), in a reverse way by blocking the activity of the fusion protein using the tyrosine-kinase inhibitory drug imatinib mesylate [9]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.