When combined with anti-PD-1 blockade, NRTUA transformed the immunologically “cold” PDAC microenvironment into a “hot,” state of T-cell inflammation: the combination synergistically suppressed tumor volume and weight, boosted tumor-specific IFN-γ production, and simultaneously depleted polymorphonuclear and monocytic myeloid-derived suppressor cells. Here, IFNG is linked to neoplasm.