In cancer patients, inactivation of BRCA1 in tumor tissue, either due to BRCA1 germline or somatic pathogenic variants, epigenetic changes, or loss of wild-type alleles, is predictive for response to crosslinking chemotherapeutic agents, such as platinum-based drugs, and to PARP-inhibitors, leading to synthetic lethality in the presence of BRCA1/BRCA2 deficiency [13, 14]. The gene discussed is BRCA1; the disease is neoplasm.