Thus, in the setting of gBRCA1/2 mutation (or presumably somatic loss of heterozygosity (LOH) for BRCA1 orBRCA2) and PARP inhibitor therapy, tumor cells cannot repair ssDNA breaks that accumulate through metabolic processes and DNA replication leading to tumor-specific lethality, whereas normal cells can use HR to repair these lesions and thus are spared. Here, BRCA1 is linked to neoplasm.