Imatinib possesses activity against non-receptor breakpoint cluster region (Bcr)-Abelson leukemia virus (Abl) tyrosine kinase that is formed as a result of a chromosome rearrangement and has been implicated in the pathogenesis of nearly all cases of chronic myeloid leukemia (CML) and acute lymphoblastic leukemia with the Philadelphia chromosome (Iqbal and Iqbal, 2014). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.