PARP inhibitors, in particular, have demonstrated synthetic lethality in BRCA‐deficient cancers, including breast and ovarian tumors harboring loss‐of‐function mutations in homologous recombination pathway genes, primarily BRCA1 and BRCA2.[126] This dual mechanism, i.e., DNA damage induction and innate immune activation via STING, presents an opportunity for enhanced therapeutic efficacy in BRCA‐deficient tumors when STING agonists and DDR‐targeting agents are used in combination. The gene discussed is STING1; the disease is ovarian neoplasm.