Editor—Chromosomal translocations that targetc-MYC at 8q24 are found in all Burkitt's lymphomas (BL), AIDS related non-Hodgkin's lymphoma (AIDS-NHL), mouse plasmacytomas (PCTs), in many examples of diffuse large cell lymphoma (DLCL), and in multiple myeloma (MM). Indications are thatc-MYC is under strict control and when deregulated results in unchecked cellular proliferation and hyperplasia. Non-random chromosomal translocations found such as t(8;14), t(8;22), or t(2;8) in these lymphoid neoplasias placesc-MYC under the control of strong immunoglobulin enhancers, which leads to overexpression.1 ,2 In addition,c-MYC is amplified in many tumours including breast, prostate, gastrointestinal, ovarian, MM, myeloid leukaemia, and melanoma suggesting that the overall transcriptional level is probably a key transforming element associated withc-MYC.3 Besides genetic lesions, other epigenetic factors such as activation of growth factor receptors may also lead to constitutive expression ofc-MYC. Thus, considerable efforts have been made systematically to identify the c-MYCtranscriptional apparatus (promoters and enhancers) in an effort to control c-MYC expression. Whilec-MYC transcription potentially initiates from one of three promoters, P0, P1, and P2 which reside in the exon 1 region, the P2 promoter normally accounts for 75-90% of cytoplasmicc-MYC RNAs. To date, more than 20 transcription factors have been found to reside in the proximity of exon 1 of c-MYC. 1 Actually,c-MYC was one of the first genes to exhibit transcriptional blockage. RNA polymerase II initiation complexes were shown to pause on P2 before activation.4-6 Upon chromosomal translocation, the insertion of IG enhancer elements renders a shift in promoter usage from P2 towards P1 and loss …