Strikingly, rather than activating canonical NF-κB or type I IFN signalling, cGAS–STING activity in CIN-high TNBC cells was shown to preferentially activate the metastasis-promoting non-canonical NF-κB (NC-NF-κB) pathway [115, 116], suggesting that tumour cells can rewire their cGAS–STING signalling circuitry to co-opt its pro-tumour signalling arms. The gene discussed is CGAS; the disease is neoplasm.