The implications of this are two-fold: 1) BRCA2 mutation status (and by extension HRR-proficiency) is heterogeneous, even in tumor populations primarily composed of BRCA2-mutated cells and; 2) the selection pressure for HRR proficiency is so great during PARP1 inhibitor treatment that tumor cells with functional HRR have a distinct survival advantage and will eventually overtake the HRR-deficient population. This evidence concerns the gene PARP1 and neoplasm.