Consistent with this notion, our data demonstrate that a-PDL1-TGFβRII is significantly more effective in inhibiting tumor progression compared with the corresponding a-PD-L1 antibody due to its bifunctional ability to not only block PD-L1/PD-1 interaction, but simultaneously interrupt autocrine/paracrine TGF-β signaling in the localized microenvironment of PD-L1 expressing tumor-infiltrating immune cells and tumor cells. Here, CD274 is linked to neoplasm.