Chronic myelogenous leukemia (CML) serves as a valuable paradigm for understanding the molecular genetic origins of cancer. The cytogenetic standard of diagnosis, the Philadelphia chromosome, has been superseded by a molecular definition for the disease, that of BCR/ABL gene rearrangement. The use of BCR/ABL to recreate CML in mice fulfills Koch's postulates for molecular pathogenesis. The present murine systems facilitate research into the biology of BCR/ABL-induced leukemias, but fall short in their promise to provide models for testing new therapies for CML. A transgenic strain of mice with an inheritable predisposition to CML would be an invaluable tool.