In the present study, we found that EBV infection led to the upregulation of CXCL8 in GC cells and CXCL8 expression promotes VM formation, which, however, was inhibited by CXCL8 knockdown, indicating that CXCL8 is involved in VM formation in EBVaGC. This evidence concerns the gene CXCL8 and Epstein-Barr virus infection.