About 20% of TNBCs are BRCA1 (breast cancer 1, early onset) mutated, and some TNBCs demonstrate functionally BRCA1-mutation-like molecular characteristics and behavior; the BRCA1 protein and another enzyme, PARP (poly (ADP)-ribose polymerase) are stimulated by single- and double-strand DNA breaks and play a significant role in maintenance of genomic stability [6], [10]. This evidence concerns the gene BRCA1 and breast carcinoma.