These leukemic cells contain a characteristic t (9:22) translocation resulting in the fusion of the Abelson (ABL) oncogene to the breakpoint cluster region (BCR) gene, and thus express a constitutively activated fusion protein BCR-ABL1, a tyrosine kinase, that is involved in the pathogenesis of CML [1]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.