Our results showed that MET reduced intracellular ATP production by decreasing the mitochondrial oxidative phosphorylation level in polycystic kidney epithelial cells; MET can inhibit the proliferation of polycystic kidney epithelial cells by activating AMPKα activity (increase in the phosphorylated AMPKα level) and inhibiting mTOR pathway activity (decrease in the phosphorylated mTOR, p70 S6K and 4E-BP1). This evidence concerns the gene MTOR and polycystic kidney disease.