The origin of many blood cancers has been shown to result from the dysregulation of critical oncogenes as a result of chromosomal rearrangements within the tumor cells. In the first few cases that these oncogenes have been specifically targeted, we have been able to develop more specific, effective, and less toxic therapy (eg, Gleevec). In multiple myeloma we have identified similar translocations and oncogenes, and we now propose to study their contribution in the pathogenesis of multiple myeloma hoping that they may represent novel therapeutic targets.