Aldosterone freely crosses phospholipid membranes and binds to the cytosolic mineralocorticoid receptor (MR) (1). The aldo/MR complex translocates to the nucleus, binds to specialized hormone response elements (HREs), and promotes the transcription of aldosterone-regulated genes, including SGK1, which is translated into protein (2). Newly synthesized SGK1 up-regulates ENaC activity through several distinct pathways that reduce ENaC ubiquitination through bi-phosphorylation of Nedd4-2 (3), prevent ENaC endocytosis by phosphorylation of WNK4 (4), recruit silent ENaC channels to active ones by direct phosphorylation (5), and inhibit the transcriptional repressor complex Dot1a–AF9 via phosphorylation of AF9 (6).