While there was a statistically significant reduction in tumor size compared to control tumors, the effect of olaparib on Brca1-deficient breast tumors was modest, in contrast to its remarkable effect on a comparable mouse model of high-grade serous ovarian cancer (HGSOC) driven by concurrent ablation of Brca1 and Trp53 and overexpression of cMyc (referred as PBM), where we found that the ovarian tumors had a dramatic response to olaparib with a robust activation of anti-tumor CD8+ T cell response in the TIME, which was essential for the therapeutic efficacy of PARPi16. The gene discussed is BRCA1; the disease is breast neoplasm.