CGAS and neoplasm: Recent studies have identified the cGAS-STING pathway and thesubsequent release of type I interferons as key mediators of radiation-inducedimmune stimulation. However, this effectis limited by the radiation-induced activation of Trex1, a DNA exonucleasethat degrades cytosolic DNA, thereby dampening cGAS-STING activationat higher radiation doses. Our data suggestthe potential of combining radiation with FA-SCNPs, which enhancesthe release of tumor-associated antigens through direct cell killingand amplifies the cGAS-STING signaling by modulating cellular calciumlevels.