BRCA1/2-mutated HGSOCs exhibit a higher mutational load and a unique mutational signature thus harboring more tumor-specific neoantigens that stimulate recruitment of an increased number of tumor-infiltrating lymphocytes (TILs), which is counterbalanced by overexpression of immune checkpoints such as PD-1 or PD-L1. The gene discussed is BRCA1; the disease is neoplasm.