Active PKR, TBK-1, cGAS/STING, and RIG-I all have the potential to restrict Δγ134.5 replication [14,15,16,41], and the heterogenous inhibition of these pathways across cancer types provides a possible explanation for the replication variability observed with first-generation Δγ134.5 oncolytics. Here, STING1 is linked to cancer.