Indeed, using genetically engineered EBV, lacking individual EBNA-3 ORFs, EBNA-3A and -3C but not -3B blocked Bim mediated apoptosis in response to multiple cytotoxic drugs in a BL derived cell line, providing a possible explanation by which EBV contributes to BL-pathogenesis (Anderton et al., 2008). This evidence concerns the gene BCL2L11 and Burkitt lymphoma.