Of interest, upon triggering of EBV reactivation from Akata cells, a significant increase in cleaved caspase-3 was seen in METTL3 KO cells compared to wild-type Akata cells, suggesting that METTL3-mediated m6A methylation contributes to suppression of apoptotic cell death during lytic EBV infection (65). This evidence concerns the gene METTL3 and Epstein-Barr virus infection.