GlcNAc6ST-1 mediates sulfation of C6 position of GlcNAc residue, which is an essential step for KS biosynthesis.12 Therefore, GlcNAc6ST-1-deficient (GlcNAc6ST-1−/−) mice show loss of KS in the CNS.13 We and others reported14, 15, 16 that KS expression is enhanced in microglia/macrophages and the extracellular matrix after spinal cord injury (SCI). This evidence concerns the gene CHST2 and spinal cord injury.