We demonstrate that use of this bivalent nanobody carrier for STING agonist delivery further increases tumor accumulation while also inhibiting immunosuppressive PD-1/PD-L1 interactions, resulting in a reprograming of the tumor microenvironment (TME) to a more immunogenic “hot” milieu and a priming of antitumor T cells that further potentiate responses to multiple immunotherapeutic modalities. The gene discussed is CD274; the disease is neoplasm.