A role for the p52 NF-kappaB subunit in tumorigenesis has been steadily emerging since its discovery as a gene associated with chromosomal translocations in B- and T-cell lymphomas. Now Eliopoulos and co-workers have extended these studies to examine the effect of the Epstein-Barr virus (EBV)-encoded latent infection membrane protein 1 (LMP1) on p52. They find that LMP1 stimulates the processing of p100 to p52 NF-kappaB. Moreover, nuclear p52 is also associated with LMP1 expression in tumor tissue biopsies. They also demonstrate that the pathway leading to p100/p52 processing is distinct from that engaged by LMP1 to activate other NF-kappaB subunits through IkappaBalpha degradation. A clearer picture is now developing of the important role that p52 NF-kappaB plays during normal cell growth and how subverting its function can contribute to oncogenesis.