Multiple myeloma is a clonal neoplasm of terminally differentiated B cells which accounts for about 1% of new cancers.1 Despite an increased understanding of the biology of the malignant plasma cell, myeloma remains incurable with current chemotherapy. Although multiple myeloma is highly sensitive to chemotherapy, combination chemotherapy regimens have not achieved better outcomes than achieved by melphalan and prednisone therapy.2 Large comparative studies have demonstrated superior response rates, overall survival, and event-free survival using high-dose therapy and autologous Stem cell transplant (SCT) compared with conventional therapy.3 Despite the improved outcome after autologous transplantation, long-term disease-free survival remains disappointingly low at 15-20%, with disease relapse being the primary reason for treatment failure.4 Myeloablative allogeneic stem cell transplantation achieves long-term disease-free survival in 15-20% patients with myeloma. The curative potential of allografting is based upon two principles. First, high-dose myeloablative therapy may eradicate disease, and hematopoiesis is restored using a tumor-free stem cell allograft. Second, donor cells mediate an immunologic antitumor effect that eradicates minimal residual disease (MRD) posttrans-plant. This immunologic effect has been termed the "graft-versus-leukemia (GvL) effect" or, in multiple myeloma, the graft-versus-myeloma (GvM) effect. For allogeneic SCT to achieve its full potential in the treatment of patients with myeloma, efforts are now being directed toward both reducing the attendant toxicity of allogeneic SCT and enhancing the GvM effect after transplant. Identification of the mediators and targets of the GvM effect may allow for more directed immunotherapy for myeloma in the future.

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