Notably, BRCA1/2-mutated high-grade serous ovarian cancers (HGSOCs) exhibit a higher mutational load and a unique mutational signature with a significantly increased number of tumor-infiltrating lymphocytes (TILs), as well as elevated expression of programmed cell death (PD-1) or its ligand (PD-L1) in tumor-associated immune cells compared to homologous-recombination (HR)-proficient tumors [8,9]. This evidence concerns the gene BRCA1 and neoplasm.