Furthermore, we found that inhibiting EBV DNA replication, which is essential for the expression of late lytic genes,38 does not impede the early lytic-induced upregulation of KDM5B. Given the well-established role of KDM5B in histone modifications,25 our findings highlight the robust capability of EBV lytic infection, even at incomplete (abortive) lytic cycle that does not progress to full DNA replication and virus production,38 to induce histone modifications and drive tumor progression in EBV-positive NPC and GC cells. This evidence concerns the gene KDM5B and gastric cancer.