SGK1 and experimental autoimmune encephalomyelitis: Recent studies have shown that high-salt could aggravate the severity of experimental autoimmune encephalomyelitis (EAE) by inducing a Th17 cell immune response, whereby the effect of high-salt on Th17 cell polarization was mediated by activating the p38/MAPK pathway via nuclear factor of activated T cells 5 (NFAT5) and serum/glucocorticoid-regulated kinase 1 (SGK1) [19, 20].