Background <p>Although genome-wide promoter CpG island hypermethylation of Epstein–Barr virus-associated gastric carcinoma (EBV GC) is well known, <i>ZNF793</i> is rarely methylated in EBV GC but is frequently methylated in other molecular subtypes of GC, including microsatellite instability-high GC. Based on the hypothesis that ZNF793 may be important for cell survival and stemness in EBV GC, the oncogenic role of ZNF793 was investigated. </p> Methods <p>ZNF793 expression was knocked out and then restored in EBV and non-EBV GC cell lines, and its effects on cell proliferation, cell migration, cell invasion, tumor sphere formation, and xenograft tumor formation were assessed. </p> Results <p>ZNF793 knockout significantly suppressed the migration, invasion, proliferation, and stemness in GC cells with ZNF793 expression. Additionally, ZNF793 knockout significantly inhibited tumor growth in a xenograft tumor model.</p> Conclusions <p>These results suggest that ZNF793 plays an oncogenic role in not only EBV GC but also other subtypes of GC and may be a potential therapeutic target.</p>