Genomically unstable cancer cells can mitigate the deleterious, immune-mediated consequences of tumour cell-triggered inflammation, in part through suppression of the type I IFN response.31 Indeed, tolerance of continuous genomic segregation errors likely represents an evolutionary bottleneck that ultimately promotes both cellular invasion and metastasis.31 Unlike normal cells, cancer cells largely respond to chronic cGAS-STING activity through the non-canonical p52/RelB NF-κB pathway,57 which critically lacks type I IFN signalling capacity. This evidence concerns the gene CGAS and neoplasm.