Mouse plasmacytomas and human Burkitt lymphomas are marked by characteristic chromosomal translocations involving the c-myc gene on one chromosome (murine chromosome 15, human chromosome 8) and the IgH locus on a second chromosome (murine chromosome 12, human chromosome 14). These result in the conversion of the c-myc gene from a normal cellular gene into the c-myc oncogene (reviewed in [1]). The formation of the myc oncogene is generally brought about by divorce of c-myc coding sequences, located in its exons 2 and 3, from exon 1 and upstream regulatory regions, coupled with the juxtaposition of myc coding sequences o immunoglobulin heavy chain (IgH) gene sequences (Fig. 1). (The reciprocal product, involving myc exon 1 and its upstream regulatory sequences, is not required for malignant transformation). Thus, the formation of the myc oncogene involves not only loss of its normal regulatory elements but also the acquisition of different regulatory influences associated with its new, immunoglobulin-associated, chromosomal environment. The focus of this paper is on the nature of IgH associated sequences that impact upon the c-myc oncogene in B cell malignancies.