In cyst-lining epithelial cells of ADPKD patients and mouse model experiments, the mammalian target of rapamycin (mTOR) pathway was shown to be activated, which may result from loss of PC1 binding with tuberin, suggesting that PC1 inhibits cell proliferation by downregulating mTOR activity through interaction with tuberin [18]. This evidence concerns the gene TSC2 and autosomal dominant polycystic kidney disease.