Although the mechanisms responsible for CML disease progression are still largely unclear, growing evidence suggests that the phenotype of CML-BC cells depends on the unrestrained activity of BCR/ABL and on the genetic or functional inactivation of genes with tumour suppressor activity (Calabretta and Perrotti, 2004). Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.