This is in agreement with the observation that PHA-II patients with WNK4 mutations exhibit changes in epithelial potential difference and conductance that resemble mild CF, which could be explained by the ability of mutant WNK4 to suppress the the epithelial sodium channel (ENaC) or CFTR in nasal epithelia and sweat ducts of PHA-II patients (Farfel et al., 2005; Yang et al., 2007). The gene discussed is CFTR; the disease is pseudohypoaldosteronism type 2.