By providing the precise metabolic mechanisms for tumor initiation in a tissue-dependent manner, breast/ovarian epithelial cells from BRCA1 carriers can therefore be viewed as fertile models not only for understanding the basic metabolic mechanisms of oncogenesis, but also as idoneous clinical scenarios for how to realize the promise of personalized therapeutic approaches to metabolic cancer prevention and therapy in a much larger group of sporadic cancers. The gene discussed is BRCA1; the disease is neoplasm.