Two other studies in BRCA1-deficient breast cancers and BRCA1/2-deficient ovarian cancers, respectively, demonstrated that these tumors may have higher predicted neoantigen loads, more tumor-infiltrating lymphocytes and increased expression of PD-1 and CTLA-4 as compared to their homologous-repair–proficient counterparts [27, 28]. This evidence concerns the gene CTLA4 and breast carcinoma.