In line with this, it was recently shown that high radiation doses induce the exonuclease Trex1, which degrades cytoplasmic DNA and downmodulates cGAS-STING pathway, thus attenuating cancer immunogenicity; on the other hand, low dose radiotherapy (LDRT) effectively induces cytoplasmic DNA accumulation without Trex1 induction, and this efficiently stimulates IFNβ production and T-cell priming, enhancing the response to immunotherapy (83). The gene discussed is TREX1; the disease is cancer.