The STING pathway is a key innate immune signaling pathway that detects cytosolic DNA and cyclic dinucleotides (CDNs), triggering the production of type I interferons (IFNs) and pro-inflammatory cytokines. This pathway is essential for host defense against pathogens and for the development of antitumor immune responses. STING, a protein associated with the endoplasmic reticulum (ER), is activated by CDNs generated by bacteria or by cytosolic DNA bound to cyclic GMP-AMP synthase (cGAS). Once activated, STING forms a complex with TBK1, which traffics to perinuclear regions to phosphorylate transcription factors like IRF3 and NF-κB, leading to the induction of innate immune genes. STING signaling is also involved in autoinflammatory diseases such as systemic lupus erythematosus (SLE) and Aicardi-Goutières syndrome (AGS), where mutations in STING or related genes lead to chronic STING activation and excessive cytokine production. STING signaling is independent of other DNA sensing pathways like TLR9 and AIM2, and it plays a crucial role in both innate and adaptive immunity. It is involved in the recognition of DNA viruses, retroviruses, and bacterial pathogens, and its activation can lead to the production of type I IFNs, which are important for antiviral and antitumor responses. However, in some cases, STING activation can promote bacterial survival by downregulating host defense responses. STING is also involved in the regulation of mitochondrial DNA (mtDNA) and the clearance of apoptotic cells, which helps prevent the activation of innate immune pathways by self-DNA. STING signaling is essential for the development of adaptive antitumor immunity, as it facilitates the priming of cytotoxic T lymphocytes (CTLs) and the cross-presentation of tumor antigens. STING agonists, such as CDNs and certain compounds like DMXAA, have shown promise in antitumor therapies. However, their efficacy is limited by differences in human STING structure compared to that in mice. Understanding the role of STING in immune responses and disease pathogenesis may lead to the development of new therapeutic strategies for cancer, autoinflammatory diseases, and infectious diseases.The STING pathway is a key innate immune signaling pathway that detects cytosolic DNA and cyclic dinucleotides (CDNs), triggering the production of type I interferons (IFNs) and pro-inflammatory cytokines. This pathway is essential for host defense against pathogens and for the development of antitumor immune responses. STING, a protein associated with the endoplasmic reticulum (ER), is activated by CDNs generated by bacteria or by cytosolic DNA bound to cyclic GMP-AMP synthase (cGAS). Once activated, STING forms a complex with TBK1, which traffics to perinuclear regions to phosphorylate transcription factors like IRF3 and NF-κB, leading to the induction of innate immune genes. STING signaling is also involved in autoinflammatory diseases such as systemic lupus erythematosus (SLE) and Aicardi-Goutières syndrome (AGS), where mutations in STING or related genes lead to chronic STING activation and excessive cytokine production. STING signaling is independent of other DNA sensing pathways like TLR9 and AIM2, and it plays a crucial role in both innate and adaptive immunity. It is involved in the recognition of DNA viruses, retroviruses, and bacterial pathogens, and its activation can lead to the production of type I IFNs, which are important for antiviral and antitumor responses. However, in some cases, STING activation can promote bacterial survival by downregulating host defense responses. STING is also involved in the regulation of mitochondrial DNA (mtDNA) and the clearance of apoptotic cells, which helps prevent the activation of innate immune pathways by self-DNA. STING signaling is essential for the development of adaptive antitumor immunity, as it facilitates the priming of cytotoxic T lymphocytes (CTLs) and the cross-presentation of tumor antigens. STING agonists, such as CDNs and certain compounds like DMXAA, have shown promise in antitumor therapies. However, their efficacy is limited by differences in human STING structure compared to that in mice. Understanding the role of STING in immune responses and disease pathogenesis may lead to the development of new therapeutic strategies for cancer, autoinflammatory diseases, and infectious diseases.