The translocation fuses the BCR and ABL genes, which results in the production of oncoprotein with an aberrant tyrosine kinase, which confers proliferative and survival properties to hematopoietic cells [3].This kinase plays a critical role in the pathogenesis of CML by activating multiple signaling pathways such as Ras, PI3K, MAPK, JAK/STAT, and Myc [4]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.