To overcome the limitations of traditional STING agonists, which do not work in STING-silenced cancers [31,36,37], we explored the idea of introducing naturally occurring constitutively active gain-of-function STING mutants [38,39] to reactivate antitumor immunity in STING-silenced, immunologically “cold” PDAC. The gene discussed is STING1; the disease is cancer.