NFAT5 and rheumatoid arthritis: Similar to the pathogenic pathway of RA, high salt results in increased p38-MAPK and NFAT5 expression in this model, promoting the expression of SGK1, a downstream target of NFAT5 (54, 57), indicating that EAE is dependent on a high salt-NFAT5-SGK1- TH17 axis.