SLC12A3 and pseudohypoaldosteronism type 2: The discovery that the lysine kinases (WNK) (1) and the ubiquitin ligases involved in their degradation (2) were the target of genetic mutations that result in clinical manifestations of type II pseudohypoaldosteronism, whose symptoms can be alleviated by inhibition of the sodium-chloride cotransporter (NCC), was a significant trigger for the interest in the participation of distal convoluted tubules in the preservation of electrolyte homeostasis.