BCR/ABL-induced chronic myeloid leukemia (CML) is a stem cell-induced but progenitor cell-driven disease, which usually starts as a relatively benign chronic phase (CML-CP), eventually progressing to a fatal blast crisis (CML-BC). 1 The frequency of additional chromosomal abnormalities is approximately 7% in CML-CP and increases to 40–70% in the advanced phases. 2 In addition, chromosomal aberrations have also been found in leukemia cells resistant to dasatinib and/or imatinib, and in patients relapsing after hematopoietic transplantation. 3, 4 The most frequently noticed chromosomal errors involve numerical gains and losses of chromosomes, isochromosome i (17q) causing loss of p53, reciprocal translocations 3; 21 and 7; 11 generating AML-1/Evi-1 and NUP98/HOXA9 fusion proteins, respectively, and other translocations and inversions associated with AML/myelodysplasia, such as inv (3) and t (15; 17). 5 Clinical and experimental observations strongly