As a result, STING agonist administration enhances the expression of IFN-β and other proinflammatory cytokines (e.g., IL-6 and TNF-α) or chemokines (e.g., CCL2/3/4/5 and CXCL9/10), the maturation and functions of DCs, and the expansion of tumor-infiltrating CD8+ T cells [106]. This evidence concerns the gene STING1 and neoplasm.