Cancer arises from genetic alteration of the pathways that regulate the balance between cell proliferation and cell death. For many blood cancers this occurs from the dysregulation of crticial oncogenes as a result of chromosomal rearrangements within the tumor cells. By specifically targeting these oncogenes we have been able to develop more specific, effective and less toxic therapy (e.g. Gleevec in CML). In multiple myeloma (MM) we have identified similar translocations and oncogenes, and we now propose to study their contribution to the pathogenesis of MM and their mechanism of action hoping that they may represent novel therapeutic targets.