Thus, dependence on BCR/ABL expression is not only a characteristic of CML-CP but also of CML-BC; however, BCR/ABL-independent mechanisms also seem to contribute to disease progression and imatinib resistance in some CML cases (Donato et al, 2003; Dai et al, 2004). This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.