We previously identified a STING-driven chemokine response signature in DNA repair-deficient breast cancers, which was associated with improved outcome in the context of standard-of-care chemotherapy.13 However, chronic stimulation of cGAS-STING via micronuclei in chromosomally unstable cancers results in inactivation of interferons and instead promotes downstream NFκB-RelB-mediated metastasis.3 The intrinsic STING activation or suppression inherent in cancer is a therefore a potential predictive biomarker for immune or other therapies. This evidence concerns the gene STING1 and breast carcinoma.