We treated ex vivo glioma tumor slice cultures with PVSRIPO alongside known canonical type-I IFN inducing PRR agonists: Poly(I:C) [TLR3 agonist13]; Lipopolysaccharide [LPS; TLR4 agonist14]; and 2′3′-cGAMP [cGAMP; STING agonist15] to define the inflammatory impact of engaging diverse PRR signaling pathways. The gene discussed is STING1; the disease is neoplasm.