BRCA1/2 mutational loss of function is a primary driver of epithelial ovarian cancer and is the basis of therapeutics targeting a synthetic lethality mechanism of poly (ADP-ribose) polymerase (PARP) inhibition in combination with BRCA1/2 mutation or possibly other homologous recombination genetic deficiencies [1, 2]. Here, BRCA1 is linked to ovarian carcinoma.