In most cases, ADPKD is induced by loss of function mutations affecting the nonselective calcium channels polycystin 1 or polycystin 2 (TRPP2, PKD2, PC2), which are physiologically involved in the regulation of various cellular functions including fluid transport, differentiation, proliferation, cell adhesion, and apoptosis [155,156]. This evidence concerns the gene PKD2 and autosomal dominant polycystic kidney disease.