The BCR/ABL fusion gene is pathognomonic for the human disease chronic myeloid leukae-mia (CML). CML is a malignant myeloprolif-erative disorder that is characterised at the cytogenetic level by the Philadelphia (Ph) translocation between chromosomes 9 and 22. At the molecular level this results in the juxta-position of parts of the BCR and ABL genes to form a fusion gene (that is, BCR/ABL). The p21O0cr/abl protein tyrosine kinase product of BCR/ABL is presumed to be responsible for the biological and clinical features of CML in humans. A vast amount of work has been done on the molecular biology and biochemistry of p21 0lcr abl (reviewed in'2) but this article is con-cerned with the cell biological consequences of p21 obcr abl expression.