ATM and Fanconi anemia: Members of the Fanconi anaemia family, such as RAD51C, RAD51D, and BRIP1, have germline or homozygous somatic mutations that increase susceptibility to HGSOC [64,65], and pre-clinical studies have proven that defects in these genes, as well as probably other HRR-associated genes, such as ATM, CHEK1, CHEK2, and CDK12, also impart sensitivity to DNA repair inhibition [34,64,66].