Mutation of the CtBP binding motifs in EBNA 3A and 3C removes their ability to function as co-operative oncogenes in transformation assays and delays outgrowth of immortalized cells on primary infection [46], [50], [53].The epigenetic repression of p16INK4a by EBNA 3A and 3C via CtBP has recently been shown to be a crucial step in the EBV transformation process [53], [62]. This evidence concerns the gene CDKN2A and infection.