SGK1 and myeloid sarcoma: In an experimental EAE model (Pelletier and Hafler, 2012), increased expression of p38MAPK and SGK1, enhanced induction of Th17 cells, and elevated levels of oxidative stress exacerbated the clinical symptoms of EAE (Wang et al., 2017), implying that the p38MAPK-SGK1 pathway exerts a negative effect on the treatment of MS.