In normal and adult kidney, PC1 functions by inducing the formation of PC1-tuberin-mTOR complex thereby inhibiting mTOR activity [47], yet in human ADPKD patients and mouse models, null of PC1 leads to the inability to assemble this inhibitory complex thereby causing mTOR pathway inappropriately activated [48], [49]. This evidence concerns the gene MTOR and autosomal dominant polycystic kidney disease.