Rather than the wholesale loss of STING protein from cancer cells, our data argue that the most parsimonious path toward tumour progression and metastasis is adaptive re-wiring of signalling downstream of STING—a process that can occur within days, thereby allowing tumours to simultaneously eschew the deleterious pro-inflammatory role of type I IFN while benefiting from immune-suppressive ER stress signalling (Fig. 5g). This evidence concerns the gene STING1 and neoplasm.