Transplantation experiments in the C57BL/KaLwRij mouse model of idiopathic paraproteinemia (IP) showed that an IP-producing clone can be further propagated in young, lethally irradiated mice and in nonirradiated recipients by a bone marrow and/or spleen cell transfer. The latency period before the original paraprotein was detected in the sera of recipients varied in different experiments between 1 and 9 mo. after transplantation. With subsequent transplantations, the take frequency gradually decreased. Propagation of IP for 3-4 generations may be the final limit. In comparison to age-matched control groups, no substantial influence of the transplanted IP on the survival of the recipients was observed. Transplantation of cells from mice with a B [bone marrow-derived] cell lymphoma or a myeloma led to continuous propagation of the malignancy, with a high take frequency, progressive development of the paraproteinemia and a shortened survival time of the recipients. IP represents in its final stage in the aging C57BL mice an intrinsic cellular defect within the affected B cell clone, which is different from that found in B cell malignancies.