It was first shown that chromosome segregation defects in the context of CIN could cause a deleterious, metastasis-promoting tumour cell-autonomous response to cytosolic DNA via the activation of non-canonical NF-κB signalling and inflammatory pathways downstream of STING—to the detriment of a type I interferon response [17]. This evidence concerns the gene STING1 and cervical squamous intraepithelial neoplasia.