Chronic myelogenous leukemia (CML), a clonal myeloproliferative disorder in adults, and some pediatric and adult acute lymphoblastic leukemias (ALLs) are characterized by the presence of a Philadelphia chromosome, t(9;22)(q34;q11) (1). In this chromosomal translocation, exons from a major breakpoint cluster region (M-bcr), located on chromosome 22q11, are joined to the c-abl proto-oncogene, located on chromosome 9q34. When this chromosomal translocation occurs in a hematopoietic stem cell, the resulting BCR/abl fusion protein has increased tyrosine kinase activity and a transforming capacity that is critical to the pathogenesis of these leukemic disorders.