Imatinib was the first tyrosine kinase inhibitor (TKI) designed to interfere with kinase activity of p190 and p210 oncoproteins, generated by the chimeric gene BCR-ABL, originating from translocation between terminal fragment of chromosome 9 and chromosome 22, that generates the Philadelphia chromosome (Ph+), the typical marker of chronic myeloid leukemia (CML) [4]. This evidence concerns the gene EVPL and chronic myelogenous leukemia, BCR-ABL1 positive.