By demonstrating that EBV infection leads to a significant down-regulation of Bim mRNA levels and that the reduction in Bim protein does not appear to depend on ERK signalling [4], proteasome function or changes in Bim mRNA turnover (this study), we have focused attention on Bim transcription as the primary target of EBV. Here, BCL2L11 is linked to Epstein-Barr virus infection.