Taken together, these findings indicate that, in the context of the jck mutation, a state of hyperproliferation of the cyst-lining epithelial cells ensued, in part, via increased p-ERK1/2, p-AKT, and mTOR activity, recapitulating rather precisely the ADPKD phenotype (26). This evidence concerns the gene AKT1 and autosomal dominant polycystic kidney disease.