The cyclic GMP–AMP synthase–stimulator of interferon genes (cGAS–STING) pathway is an essential component of the innate immune system and is central to the identification of abnormal DNA leakage caused by ionising radiation (IR) damage. Cell‐intrinsic cGAS–STING initiation has been revealed to have tremendous potential for facilitating interferon synthesis and T‐cell priming. Targeting the cGAS–STING axis has been proposed as a strategy to improve radiosensitivity or enhance immunosurveillance. However, due to the complex biology of the irradiated tumour microenvironment and the extensive involvement of the cGAS–STING pathway in various physiological and pathological processes, many defects in this strategy limit the therapeutic effect. Here, we outline the molecular mechanisms by which IR activates the cGAS–STING pathway and analyse the dichotomous roles of the cGAS–STING pathway in modulating cancer immunity after radiotherapy (RT). Then, based on the crosstalk between the cGAS–STING pathway and other signalling events induced by IR, such as necroptosis, autophagy and other cellular effects, we discuss the immunomodulatory actions of the broad cGAS–STING signalling network in RT and their potential therapeutic applications. Finally, recent advances in combination therapeutic strategies targeting cGAS–STING in RT are explored. Ionising radiation (IR)‐induced activation of the cGAS–STING cytosolic nucleic acid sensing pathway has a dichotomous role in initiating cancer immunosurveillance and immunosuppression, which is critical for remodelling the tumour microenvironment. Other signalling events activated after IR, such as various cell death modalities, can further regulate cancer immunity indirectly by enhancing or inhibiting cGAS–STING signalling. Therefore, targeting the cGAS–STING pathway in radiotherapy (RT) to enhance antitumour immune activation without causing negative effects such as immunosuppression and RT resistance is a promising combination therapy approach.