Consistent with a polycystin-dependent inhibition pathway, reactivation of Pkd1 or Pkd2 transgenic expression after induced loss of the endogenous genes in kidney tubules showed that the cystic phenotype can be halted or even reversed by re-expression of the ADPKD genes.102 These results have important implications for future therapies re-expressing the ADPKD gene or repairing the endogenous defect. Here, PKD2 is linked to autosomal dominant polycystic kidney disease.