STING1 and glioblastoma: Cancers have been shown to employ these mechanisms, and others, to inhibit translocation of activated immune response mediators such as STING, through epigenetic changes (i.e., hypermethylation of the STING promoter), and by selecting for the expansion of cell with specific mutations, such as those affecting IFN receptor.79–82,95–98 Due to the multiple factors promoting GBM growth, treatment for these tumors will likely require multimodal strategies targeting multiple immune response pathways.