In this study, researchers observed that NDV alone enhanced effector T cell phenotypes but did not yield effectual tumor control, and further investigations revealed that NDV promoted PD-L1 production in the tumor milieu through distinct mechanisms, including augmented expression of PD-L1 occurred in virus-infected tumors as a response to virus-stimulated type I IFN signaling in a paracrine fashion, and in distant tumors as an adaptive immune resistance against increased tumor-infiltrating immune cells [69]. Here, CD274 is linked to neoplasm.