In this context, it is proposed that ADPKD and ARPKD arise from decreased LATS1/2 phosphorylation and increased YAP/TAZ transcriptional activity, while, conversely, increased LATS1/2 signaling and reduced cellular proliferation underlie the NPH forms (reviewed in ref. 10). This evidence concerns the gene LATS1 and autosomal recessive polycystic kidney disease.