Using a genetically engineered mouse model (GEMM) of Brca1-deficient ovarian cancer, we showed that treatment with PARPi leads to release of double-stranded DNA (dsDNA) fragments by tumor cells, which activate stimulator of interferon genes (STING) signaling in intratumoral dendritic cells (DCs), thus triggering a type I interferon (IFN) response and subsequent induction of anti-tumor CD8+ T cells16. Here, BRCA1 is linked to neoplasm.