Moreover, a chemically induced point mutation in the SAM domain of ANKS6 that impairs its recruitment to Bicc1 in cystic kidneys of ANKS6I747N/I747N mice has been shown to diminish the accumulation of polycystin-2 [13], a phenotype that is reminiscent of Bicc1 loss-of-function [34]. Here, ANKS6 is linked to Renal cyst.