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Chronic myeloid leukemia (CML) was the first human malignancy shown to be consistently associated with a chromosomal abnormality,the Philadelphia chromosome.At the gene level,the Philadelphia chromosome is the result of breaks on chromosomes 9 and 22 with a reciprocal translocation of the distal genetic material.This translocation forms the new hybrid BCR-ABL oncogene,an abnormal 8.5-kb RNA that encodes a 210-kDa fusion protein,which,presumably through its increased tyrosine kinase activity,changes normal hematopoietic cells into CML cells [1].