The regular activation of the c-myc oncogene by juxtaposition to one of the immunoglobulin loci by chromosomal translocation in Burkitt's lymphoma (BL), mouse plasmacytoma and rat immunocytoma indicates that these translocations represent an essential, i.e. rate limiting step in the development of these tumors. Since the myc-carrying chromosome appears to break at random, but preserves the integrity of the two coding exons, the exclusive involvement of myc (rather than other oncogenes) requires special comment. It must be relatable to the specific functional features of the precursor cells and to the normal role of the myc protein. Recent evidence indicates that the myc gene is regularly turned off before or at the time when the cell enters a pathway that is programmed to lead it towards a resting G0 state. Clonally expanded B-cells are believed to turn into resting memory cells upon waning of the antigenic stimulus. The normal, non-translocated myc-allele is regularly switched off in both BL and murine plasmacytoma (MPC), indicating that the cell has already obeyed a program that involves the down regulation of myc. The Ig-juxtaposed, translocated myc remains highly expressed, however, and may be responsible for keeping the cells in cycle. The possibility that BL and MPC may arise from candidate memory cells, rather than pre-B cells, is also suggested by the fact that all BL-tumors and derived lines make a heavy chain. Since the myc/Ig juxtaposition is a special case of a non-functional rearrangement, this is only expected if the precursor cell would have been preselected for a functional Ig-product. The memory cell hypothesis is further supported by the fact that the majority of BLs make IgM, most MPC make IgA and the rat immunocytomas make IgE. This could correspond to the most frequent type of the memory cell in the anatomical areas and under the physiological or pathophysiological conditions associated with the natural history of each tumor. This brief review is restricted to oncogene activation by chromosomal translocations in B-cell derived tumors.