It has been shown that tumors with defects in DNA repair pathways present a high mutational burden and higher levels of neoantigens.29 30 Furthermore, BRCA1/2-mutated HGS ovarian tumors have been shown to exhibit significantly increased CD3+ and CD8+ TILs.31 It is possible that the high genomic instability due to defects in BRCA1/2 may determine higher levels of transcription of antigenic ERVs, supporting a link between DNA repair defects, spontaneous expression of ERVs, immunogenicity, and ultimately, survival—though this relationship remains to be further investigated. Here, BRCA1 is linked to ovarian neoplasm.