Even within homologous recombination–deficient cancers, BRCA1 and BRCA2 loss generate non-identical phenotypes: BRCA1 deficiency is strongly associated with replication stress, cytosolic DNA accumulation, and robust cGAS–STING activation, whereas BRCA2 loss produces fewer cytosolic DNA fragments and a weaker inflammatory response due to its more specific role in RAD51 loading [30]. This evidence concerns the gene BRCA1 and cancer.