Given that the basal level of cGAS/STING signaling in tumors is suppressed, at least partially, by PRMT1-mediated cGAS methylation, PRMT1 inhibition is an attractive therapeutic choice to potentially synergize with these cytosolic DNA-elevating therapies, which might produce better immunogenicity in the tumor microenvironment for cancer patients. This evidence concerns the gene STING1 and neoplasm.