This lack of high fidelity DSB repair and reliance on alternative, more error-prone pathways in HRD neoplasms sets the stage for the lethal effects of PARP inhibitors (PARPi) in certain subtypes of breast, ovarian, and prostate cancer [7,8,12], especially tumors with mutations or silencing of BRCA1/2, RAD51, RAD54, DSS1, RPA1, NBS1, ATR, ATM, CHK1, CHK2, FANCD2, FANCA, or FANCC [12,13,14,15]. The gene discussed is BRCA1; the disease is neoplasm.