In these studies, significant antitumor synergy and tumor resolution were mediated through lymphocyte activation and modulation of multiple immunosuppressive myeloid populations to acquire an interferon response able to cooperatively suppress multiple experimental tumor types, including tumors refractory to PD-1/PD-L1-targeted therapies due to defects in MHC I expression, antigen processing and IFNγ signaling. The gene discussed is PDCD1; the disease is neoplasm.