Although downregulation of Bim is not seen in Latency I BLs, and therefore is not likely to be involved in most cases of BL, the observation with Wp-restricted BLs does lend credence to the idea that the pro-apoptotic checkpoints which regulate c-myc-induced proliferation in normal cells are targeted by secondary genetic changes and/or by EBV genes in the pathogenesis of BL. Here, BCL2L11 is linked to Burkitt lymphoma.