Secondly, it is well known that chronic myeloid leukaemia (CML) is a disease guided via a molecular defect on the BCR-ABL translocation, resulting in: activation and dysregulation of a large number of signalling pathways, including cell division changes and also genetic-abnormalities incorporation [36–40]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.