The notion that NCC is important for regulating K+ excretion is also supported by the fact that two genetic diseases, namely, Gitelman syndrome (caused by the loss-of-function of NCC) and pseudohypoaldosteronism type II (PHA II, caused by the gain of function of NCC), present with hypokalemia and hyperkalemia, respectively [11, 12]. The gene discussed is SLC12A3; the disease is pseudohypoaldosteronism type 2.