Although several reviews have examined cGAS-STING signaling in metabolic disorders, sterile inflammation, and cardiac injury [5,6,7], they predominantly focus on antiviral or tumor-related contexts and lack a systematic integration of T2DM-specific pathophysiological features—such as hyperglycemia-induced mitochondrial dysfunction, lipotoxicity, and gut dysbiosis—and their cell-type–specific activation within the cardiovascular system. The gene discussed is CGAS; the disease is Hyperglycemia.