An in vitro study showed that exogenous STING agonist DMXAA activates STING signaling, and then induces type I IFN production and IFN-stimulated gene expression [91, 92], thus the STING activated CTLs by exogenous STING agonists may mirror the response of innate cells and induce more CTLs to migrate and infiltrate into tumor microenvironment. The gene discussed is STING1; the disease is neoplasm.