Leukemias and lymphomas appear as the result of an uncontrolled proliferation of cells from the hematopoietic system at large. Thus, myeloid leukemias are constituted by proliferations of myeloid-“like” progenitor cells, whereas acute lymphoid leukemias and lymphomas result from the proliferation of lymphoid cells. In either case, an abnormal cell proliferation coupled with unbalanced differentiation is observed. However, in most cases, a normal counterpart can be assigned to the malignant clone, as defined by morphology, immunological markers, and, more recently, by specific gene rearrangements or gene expression. 1 Although leukemic cells exhibit many abnormal features, they usually express markers specific for the lineage from which they are thought to originate. The T-cell receptor and immunoglobulin gene rearrangements observed in the lymphoproliferative diseases demonstrate both the clonality and the lineage fidelity of the tumor population. 2 Such markers are not available for acute myeloid leukemias, which are usually defined by more classic criteria, when cytogenetic analysis is not available.