Expression of ubiquitous SGK1 is stimulated by hormones and cell stress. SGK1 is activated by insulin and growth factors via phosphatidylinositol-3-kinase and the 3-phosphoinositide dependent kinase PDK1. SGK1 activates ion channels (e.g. ENaC, TRPV5, ROMK, Kv1.3, KCNE1/KCNQ1, GluR6), carriers (e.g. NHE3, GLUT1, GLUT4, SGLT1, EAAT1-5, CreaT), and the Na+ /K+ -ATPase. It regulates the activity of several enzymes and transcription factors (e.g. forkhead- transcription-factor-FKHRL1, b-catenin, nuclear-factor-kappa-B NFkB). SGK1 participates in transport regulation, hormone and mediator release, excitability, cell proliferation and apoptosis. SGK1 contributes to Na+ retention and K+ elimination of the kidney, mineralocorticoid stimulation of salt appetite, glucocorticoid stimulation of gastric acid secretion, intestinal Na+ and glucose transport, insulin-dependent salt sensitivity of blood pressure, salt sensitivity of peripheral glucose uptake, insulin release, coagulation, immune response, memory consolidation and cardiac repolarization. A SGK1 gene variant (~5% prevalence) is associated with increased blood pressure and body weight. SGK1 may thus contribute to metabolic syndrome. Moreover, the gene variant is associated with shortened cardiac QT interval. SGK1 may further participate in tumor growth, neurodegeneration, fibrosis and the sequelae of ischemia.