In our case, the KLC populations have polarized polygonal epithelial morphology and large cytoplasmic extensions that might be induced or regulated by SAMSN1. Consequently we hypothesized that the defect in the 5′ UTR of the SAMSN1 gene reduced the expression of SAMSN1, which in turn affected KLC differentiation or function in ADPKD. This evidence concerns the gene SAMSN1 and autosomal dominant polycystic kidney disease.