That metformin could block cancer cell invasion and anaplasia, but not tumor growth, suggested that the molecular pathways of anti-diabetic and anticancer actions of metformin could differ in vivo. Although the detailed molecular basis underlying the metabolic effects of metformin are not completely understood, the primary molecular mechanism mediating this effect appears to be the activation of AMP-activated protein kinase (AMPK) and the subsequent inhibition of mammalian targets of rapamycin (mTOR) [43–45]. The gene discussed is MTOR; the disease is cancer.