By altering the (3’ to 5’) segment of the ABL oncogene (9q34) and BCR gene (22q11.2), respectively, the BCR-ABL fusion gene, which encodes a constitutive TK active oncoprotein.[54,55] Existing management has developed in the past and generally comprises the practice of TKIs to constrain the activity of BCR-ABL TK in CML patients triggered by Philadelphia chromosome.[56,57]. This evidence concerns the gene TKT and chronic myelogenous leukemia, BCR-ABL1 positive.