Residual disease after bone marrow transplantation (BMT) can either cause relapse or persist in a balanced state in which immune mechanisms keep control over malignant cell proliferation. After allogeneic BMT the latter mechanism [summarized as graft-versus-leukemia (GVL)] is probably supported by cellular (e.g. T lymphocytes, natural killer cells) and humoral (e.g. cytokines) effectors and often linked to clinical manifestations of GVHD. Preclinical and clinical studies are now emerging in which cytokines, such as interleukin-2 or interferons, are given after BMT to support cellular immune function particularly in situations in which GVL does not occur. We summarize here results from both pre-clinical and clinical studies that are relevant to the design of protocols seeking to improve elimination of residual malignant disease in BMT patients by modulation of the immune system.