PARP inhibitors act by multiple mechanisms, including trapping PARP on DNA at sites of single-strand breaks, thereby preventing repair of the single-strand breaks and generating double-strand breaks during DNA replication that cannot be repaired accurately in tumors that have homologous recombination deficiency (HRD), such as tumors with a BRCA mutation (BRCAm, defined as a functional deficiency in BRCA1 and/or BRCA2). The gene discussed is BRCA1; the disease is hypoparathyroidism-retardation-dysmorphism syndrome.