DEF6 and experimental autoimmune encephalomyelitis: Our previous study of Def6-deficient mice revealed SLAT to be a critical selective regulator of the TCR-coupled Ca2+/NFAT signaling pathway, controlling positively CD4+ Th cell activation and differentiation, as evidenced by its critical role in the development of T cell-dependent inflammatory diseases such as allergic lung inflammation [17] and experimental autoimmune encephalomyelitis [18].