Possible mechanisms of CML disease progression. BCR/ABL expression is sufficient to transform hematopoietic stem/progenitor cells and to induce a CML-like disorder in mice. Increased expression of BCR/ABL, frequently observed in patients with CML-BC, might promote secondary molecular and genetic abnormalities that contribute to the expansion of a cell population characterized by enhanced proliferation, increased resistance to apoptosis, and differentiation arrest.