Several recent studies have suggested a mechanism in which, upon PARPi treatment, the cancer cells induce alterations to the tumor microenvironment (TME), particularly the tumor-infiltrating lymphocytes, and these changes appear to be essential in mediating PARPi anti-tumor response in BRCA1-mutated breast cancer tumors and the overall efficacy of PARPi11–13. This evidence concerns the gene BRCA1 and breast cancer.