Preclinically, metformin-induced activation of AMPK has been shown to disrupt cross-talk between insulin/IGF-1R and G protein–coupled receptors signaling in pancreatic cancer cells, (21) and inhibit cell proliferation, reduce colony formation, and inhibit MAP kinase, AKT, and mTOR in estrogen receptor–positive and –negative, as well as ERBB2-normal and -overexpressing breast cancer cell lines (22). The gene discussed is MTOR; the disease is breast cancer.