In NSCLC, tumor cells from patients with higher disease stage or lymph node metastasis generated more TGF-β than their counterparts [61], which could not only expand the infiltration of eTregs in the TME but potentiate the immunosuppressive function by elevating the expression of inhibitory molecules B7H1 and GITRL on the surface of APC cells [62]. Here, CD274 is linked to neoplasm.