Ronzaud et al. [29] provided evidence that the inactivation of Nedd4L exons 6 to 8 in adult mouse Nedd4L-KO (Nedd4LPax8/LC1) renal tubules do not result in the Liddle-syndrome phenotype associated with elevated ENaC activity; rather, it results in a salt-sensitive Pseudohypoaldosteronism Type II (PHAII)-like syndrome that is characteristic of the upregulation of NCC, increasing blood pressure and hypercalciuria. The gene discussed is NEDD4L; the disease is Liddle syndrome.