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Abstract
Chronic myeloid leukemia (CML) is a malignant haemopoietic stem cell disorder which results in excessive production of cells of the myeloid series. It is associated with a consistent molecular abnormality, the BCR/ABL fusion gene. The product of BCR/ABL is a p210 protein tyrosine kinase but it is not known how this dictates the biological features of the disease. This review considers several key processes that can be suggested as candidate targets for the action of p210.