A recent publication shed some more light on the physiological function of NHA2 in the kidney, demonstrating that NHA2 KO mice exhibit a phenotype resembling the genetic condition in humans called Gitelman’s syndrome, resulting from loss-of function mutations or deletions of the apical thiazide-sensitive Na+/Cl− cotransporter NCC (also known as SLC12A3) present in DCT cells, and characterized by hypovolemia with secondary hyperaldosteronism, reduced blood pressure, normocalcemic hypocalciuria and a blunted response to thiazide diuretics. This evidence concerns the gene SLC9B2 and Gitelman syndrome.