CD274 and neoplasm: In addition, given that the EBV+ subtype of GC often is associated with modulation of the tumor microenvironment (TME) to evade the host immune response (such as by upregulation of PD-L1 expression by CD274 focal amplification and IFN-γ-mediated signaling, causing immunosuppression), immune checkpoint blockade arose as a promising avenue of treatment [43,44,45].