In most cases of CML, a chromosomal translocation creates Bcr-Abl, a fusion protein in which the Abelson tyrosine kinase (Abl) is stripped of its regulatory regions, leaving the kinase domain free to catalyse any substrate it comes across, triggering numerous growth pathways as a result [8]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.