The tumorigenic potential of six post-transplant B-cell lymphoproliferative disease (PTLD) lesions was evaluated in SCID mice. Three animals developed local subcutaneous B cell tumours, two of which contained Epstein-Barr virus (EBV) DNA. Two animals developed CD3 positive thymic neoplasms, and one mouse developed an uncharacterized spontaneously regressing subcutaneous tumour. Immunoglobulin gene rearrangements studies with a JH probe, and EBV clonality studies with a Bam NJ fused terminal probe, showed only one mouse tumour to be genealogically related to the corresponding clinical lesion. It is concluded that lymphoid clones which constitute human PTLD are not autonomous, but sustained by host-derived growth stimuli distinct from those operating in the SCID mouse mileu.