Our previous findings support the hypothesis that ouabain’s effects in ADPKD are due to an increase of NKA signaling secondary to the abnormally high ouabain affinity of NKA in ADPKD kidneys, as shown by the increase in ADPKD cyst growth when NKA is mutated to increase its affinity for ouabain [22]. This evidence concerns the gene TAC1 and autosomal dominant polycystic kidney disease.