IFN-γ released by tumor-infiltrating immune cells can directly induce the expression of PD-L1 by both tumor and immune cells, and EBV also leads to an increase in PD-L1 expression levels via JAK/STAT signaling.[18] It follows that PD-1-driven immune escape may play an important role in EBV, which is also immunosuppressive in the tumor immune microenvironment of EBVaGC. Here, SOAT1 is linked to neoplasm.