It is thought that hypertension in PHA2 patients may partially be the result of increased sodium reabsorption via L-WNK1/Ks-WNK1 mediated up-regulation of the thiazide sensitive sodium chloride cotransporter (SLC12A3 or NCCT) and the renal amiloride-sensitive epithelial sodium channel (ENaC, encoded by three genes: SCNN1A,B and G), and hyperkalemia by increased inhibition of the renal outer medullary potassium channel (KCNJ1) [13], [14], [15], [16], [17]. The gene discussed is SLC12A3; the disease is pseudohypoaldosteronism type 2.