Chronic myeloid leukemia (CML) afflicts approximately 1.5 per 100,000 individuals in the United States, with an estimated 5000 new cases diagnosed annually.1,2 The etiology of CML is a chromosomal aberration known as the Philadelphia (Ph) chromosome, which is created by the reciprocal translocation of chromosomes 9 and 22 (t[9;22][q34;q11]).3 The Ph chromosome leads to the expression of BCR-ABL tyrosine kinase, an oncogenic fusion protein. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.