The acute myeloid leukemias (AMLs) are a relatively heterogeneous group of diseases. However, there is growing awareness that the clinical features and subclassification of morphologic leukemia types is often highly correlated with tumor genetics. Furthermore, distinct genetic subgroups of AML are associated with improved therapeutic sensitivity and a more favorable clinical outcome. These observations have prompted suggestions for a revision of the current French-American-British leukemia classification (1), utilizing genetically defined principles (2). Three recurrent chromosomal translocations are identified in approx 25-30% of de novo adult AMLs. These include the t(15;17), associated with acute promyelocytic leukemia ([APL]; AML-M3); the inv(16) and related t(16;16), associated with AML-M4Eo; and the t(8;21), associated most commonly with AML-M2. Each of these abnormalities results in the formation of a chimeric leukemia-specific fusion gene, which is transcribed and expressed as a fusion protein. The widespread genetic deregulation caused by such fusion proteins is thought to interfere with proliferative control and cell differentiation mechanisms, leading to the leukemic state. The presence of these and other fusion gene events can be specifically and sensitively detected by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis.