In these CML-BC patients, imatinib resistance often depends on reactivation of BCR/ABL tyrosine kinase activity via mechanisms involving BCR/ABL overexpression, gene amplification or mutations that suppress imatinib-mediated kinase inhibition (i.e. E255V and G250E) or disrupt imatinib binding (i.e. T315I) (Shah and Sawyers, 2003). The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.