STAT3 is solidly linked as a driver of astrogliosis after SCI [57], such that mice with conditional STAT3 deletion in astrocytes show reductions in certain aspects of reactive astrogliosis, including cell hypertrophy, up regulation of GFAP, and scar formation in experimental SCI [57, 58] and in experimental autoimmune encephalomyelitis (EAE) [59, 60]. This evidence concerns the gene STAT3 and experimental autoimmune encephalomyelitis.