It was further proposed that the lack of ClC-K2 could be partially compensated by an upregulation of ClC-K1 in the ascending limb, thus explaining the less-severe phenotypes of patients with Bartter syndrome type 3 (classic) compared to antenatal types 1 and 2 caused by the dysfunction of the apical NKCC1 and ROMK, respectively [64,65,69]. The gene discussed is CLCNKB; the disease is Bartter disease type 3.