Formation of the BCR-ABL fusion gene coding for a constitutively active BCR-ABL tyrosine kinase via t(9;22)(q34;q11) reciprocal translocation initiates 95% of chronic myelogenous leukemia (CML), and 25% of adults and 5% of children acute lymphoblastic leukemia (ALL) [1]. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.