BRCA2 and neoplasm: More intriguingly, RAD52 depletion is also synthetically lethal with defects in BRCA1, a tumor suppressor that acts upstream of BRCA2 in HR and at the branch point in the DSB repair that promotes homology-directed DNA repair through HR or SSA over the NHEJ (non-homologous end joining) (Singleton et al., 2002).