Furthermore, nucleus architecture abnormality, including micronuclei rupture, nuclear envelope blebs, and chromatin herniations, that convert genomic instability into innate immune activation, strongly supports integrating DNA-repair modulators (PARP inhibitors, ATR inhibitors) with STING-targeted therapies, particularly in BRCA-deficient cancers where synthetic lethality can be extended to immune-mediated tumor clearance. This evidence concerns the gene STING1 and neoplasm.