On the other hand, similar to the pathological T cell signaling in XLP, SAP deficient mice had increased IFN-y production and enhanced susceptibility to experimental autoimmune encephalomyelitis (EAE, the mouse model of multiple sclerosis), possibly as a result of skewing the immune system to a Th1 mediated autoimmunity (48). This evidence concerns the gene SH2D1A and Autoimmunity.