AHI1 and cystic kidney disease: Jbn is believed to interact with and facilitate β-catenin nuclear accumulation, whilst loss of the protein resulted in a decrease in β-catenin function [52,78], with Jbn and LRP6 potentially sharing the same signalling pathway, since renal atrophy and renal cysts were seen in heterozygous Ahi1+/-; LRP6+/- and homozygote Ahi1-/- mice [79].