A review examined opportunities and pitfalls of modulating the cGAS–STING pathway in cancer therapy, outlining contexts where activation can prime antitumor immunity and scenarios where chronic signaling promotes immune suppression or tumorigenesis. The paper synthesizes preclinical and early clinical data on STING agonists and inhibitors, discusses delivery challenges, dosing windows and combinatorial strategies with checkpoint blockade, and flags biomarker needs to predict patient response. Translational teams should weigh tumor type, microenvironment and timing when pursuing cGAS–STING modulators.