The dichotomous role of PKR in tumor progression suggests that PKR is a barrier that must be overcome for efficient Δγ134.5 oHSV replication in many tumor types [44,45], and studies characterizing cGAS/STING in melanoma, colorectal, and ovarian cancer cell lines have identified that epigenetic silencing, while prevalent and measurable, is not ubiquitous [76,77,92]. This evidence concerns the gene STING1 and neoplasm.