This article discusses briefly the molecular consequences of the BCR-ABL fusion gene. It then reviews the current evidence supporting the notion that chronic myelogenous leukemia in its chronic phase is a clonal, hematopoietic, stem cell disease in which malignant hematopoietic stem and progenitor cells respond to "normal" external proliferation and differentiation stimuli, but in which such responses are altered owing to defects in the stem and progenitor cells as a result of the BCR-ABL oncogene.