Both latent infection and lytic replication of EBV have been implicated in the development of epithelial tumors.5,6 Our study reveals that EBNA1, a key latent viral protein consistently expresses across all EBV-associated cancers, collaborates with the transcription factor CEBPB at the KDM5B promoter to enhance its transcription. This evidence concerns the gene KDM5B and disease arising from reactivation of latent virus.