The ability of ZNF793 to evade DNA methylation influenced by EBV infection may be associated with its role in tumor cell stemness, which was demonstrated in the present study by the observed decrease in and reversal of intracellular stem cell marker expression, tumor sphere formation, and xenograft tumor growth upon knockout and subsequent reintroduction of ZNF793, respectively. Here, ZNF793 is linked to Epstein-Barr virus infection.