It was previously thought that the WNK4 mutations found in patients with pseudohyperaldosteronism type II (PHAII, an autosomal dominant disease characterized by hypertension, hyperkalemia, and metabolic acidosis) are loss-of-function mutations and that WNK4 activation inhibits the membrane transport of NCC (Yang et al, 2003). Here, SLC12A3 is linked to pseudohypoaldosteronism type 2.