However, mutations in TRPC1 or TRPV4 alone do not lead to ADPKD, indicating that altered intracellular Ca+2 levels alone are not sufficient to initiate cyst formation; rather, the development of ADPKD appears to be specifically associated with functional impairments in either PC1 or PC2 [52]. Here, TRPV4 is linked to autosomal dominant polycystic kidney disease.