The choice of the AMPK activator MET appears ideally suited for chemoprevention of BRCA1-associated breast cancers due to: its potential to mimic BRCA1 function in the ACCA lipogenesis pathway, including in premalignant cells; its selective toxicity to cells that have become deficient in p53, an early and hallmark event in BRCA1-associated breast oncogenesis and its potential to override aberrant signaling through the PTEN/PI3K signaling pathway to which BRCA1-associated tumors are addicted (Figure 3). This evidence concerns the gene BRCA1 and breast carcinoma.