Activation of the cGAS-STING pathway has further been described in tumours undergoing DNA damage caused by endogenous DDR defects [15, 41, 48, 64, 227–233], a phenotype that was linked to increased TILs, notably in the context of HRR and NER defects [15, 31, 41], suggesting that cGAS-STING-driven innate immune signalling in DDR-defective tumours could improve response to ICB by favouring an immunologically “hot” TME. This evidence concerns the gene STING1 and neoplasm.