Our protein-protein interaction network analysis established a mechanistic basis for this deficiency, demonstrating that the somatically mutated genes ATR, BARD1, and TP53 reside at central hubs of a network significantly enriched for “Homologous Recombination” and “Fanconi Anemia” pathways, indicating a systemic compromise of the DNA repair machinery. The gene discussed is BARD1; the disease is Fanconi anemia.