By contrast, analysis of a BRCA1-deficient, p53-deficient genetically engineered mouse model of triple negative breast cancer (TNBC) and analysis of TNBC cell lines showed that activation of the cGAS/STING pathway within the tumor increased the efficacy of PARP inhibitors through tumor cell response and increased immune activation in the tumor microenvironment, with more profound benefits in homologous recombination repair-deficient tumor cells [79]. The gene discussed is PARP1; the disease is triple-negative breast carcinoma.