Epidemiological and molecular evidence links Epstein-Barr virus (EBV) carriage to the pathogenesis of human malignancies of lymphoid and epithelial cell origin but the mechanisms of viral oncogenesis are poorly understood. Burkitt's lymphoma, a tumor occurring in both EBV-positive and -negative forms, provides a convenient model for analysis of the relative contribution of genetic changes and viral products that are expressed in the malignant cells. Here we review recent findings that highlight several mechanisms by which EBV could play an important role in oncogenesis by promoting genomic instability.