A substantial body of evidence indicates that specific chromosomal abnormalities play an important role in the genesis of certain human and animal tumors. In a number of chromosomal translocations, cellular homologues of retroviral transforming genes are located near the breakpoints, suggesting that tumorigenesis can occur by the activation of these genes. Tumor-associated chromosomal abnormalities involving c-myc have been found in both mice and men, including trisomy and translocation of myc-bearing chromosomes and rearrangement and amplification of the myc gene itself. Tumor types in which c-myc abnormalities are found are predominantly lymphocytic, but include kidney (Cohen et al., 19791, colon (Alitalo et al., 19831, and lung (Little et al, 1983) carcinomas, which would seem to indicate the importance of this gene in tumorigenesis. This importance is demonstrated in the cases of murine plasmacytoma (MPC) and human Burkitt's lymphoma (BL). Although very different in etiology, pathogenesis and stage of differentiation, these B-cell-derived tumors carry very similar translocations involving c-myc and the light and heavy chain immunoglobulin loci. Concentrating on these two lymphocytic malignancies, we will attempt to review the most current findings about the links between c-myc activation -and rearrangement and the evolution of malignancy.