BRCA1 promoter hypermethylation-induced epigenetic silencing is numbered among other mechanisms known to confer HR deficiency in EOC and is reported in approximately 10% to 20% of HGSOCs; interestingly, this epigenetic modification occurs exclusively for BRCA1 gene (not for BRCA2) and is mutually exclusive of BRCA1/2 mutations, suggesting a strong selective pressure to inactivate BRCA via either mutation or epigenetic silencing in ovarian cancer [1]. Here, BRCA2 is linked to ovarian carcinoma.