In fact, along with other frequent genetic and molecular abnormalities (e.g. double Ph1 chromosome, p53 inactivation) (Johansson et al, 2002), increased expression and activity of the BCR/ABL oncoprotein is frequently observed during CML disease progression and in blast crisis CML (Elmaagacli et al, 2000; Jamieson et al, 2004; Barnes et al, 2005b), and sustained BCR/ABL expression in myeloid progenitor cell lines induces phenotypic changes (i.e. differentiation arrest) characteristic of CML-BC (Perrotti et al, 2002). The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.