The HR-deficient/non-BRCA1/2-mutated cohort included HGSOCs with mutations in Fanconi Anemia (FA) genes, mutations in core HR RAD genes (including RAD50, RAD51 and RAD54L), mutations in DNA damage response genes involved in HR such as ATM and ATR, homozygous deletion of PTEN, amplification or mutation of EMSY, and promoter hypermethylation of BRCA1 or RAD51C. This evidence concerns the gene BRCA1 and Friedreich ataxia.