IRF3 and neoplasm: The host antitumour immune response can also be triggered by cancer-specific genomic alterations and mutations.32 For instance, as a consequence of double-stranded DNA breaks caused by the presence of inactivating mutations in DNA damage repair (DDR) genes, there might be increased levels of DNA fragments in the cytoplasm of tumour cells.64 These increased levels of DNA fragments might activate the cytosolic double-stranded DNA-sensing cGAS-STING pathway, which promotes the phosphorylation of IRF3 (see Fig. 1), thereby promoting its retention in the cytoplasm.