In fact, one study showed that RAD51C-deficient cancer cells were highly sensitivity to Olaparib, significantly inhibiting tumor growth in a xenograft model [43], whereas Loveday and colleagues [26] showed that cells deficient in RAD51D were sensitive to Olaparib in a magnitude similar to the observed by silencing BRCA2. Furthermore, the Food and Drug Administration (FDA) recently approved Olaparib for the treatment of metastatic castration-resistant prostate cancer (mCRPC) patients with pathogenic germline or somatic variants in HR repair genes, including RAD51C and RAD51D [46]. This evidence concerns the gene RAD51D and cancer.