Considering other GR mutations, it was observed that (a) heterozygous GR knockout mice, in which GR expression is reduced by half, were less sensitive to dexamethasone therapy in experimental autoimmune encephalomyelitis (59); (b) mice with selective GR depletion in T cells (GRlck-Cre) succumb to toxoplasma infection due to increased TNF and IFN-γ production by Th1 cells (60); and (c) mice with selective GR depletion in the thymocytes showed loss of the adaptive immune response and were immunocompromised (61). Here, NR3C1 is linked to experimental autoimmune encephalomyelitis.