BRCA1 and BRCA2 mutational loss of function is a primary driver of breast and ovarian cancer and is also the basis of therapeutic treatment via a synthetic lethality mechanism of poly(ADP-ribose) polymerase (PARP) inhibition in conjunction with BRCA1/2 or other homologous recombination genetic defects [1, 2]. Here, BRCA2 is linked to ovarian carcinoma.