Previous researchers have demonstrated that RGM-A is expressed in pathogenic Th17 cells in experimental autoimmune encephalomyelitis (18), and the binding of RGM-A to its receptor neogenin inhibits PMN migration and increases the attachment of CD4+ cells to intercellular adhesion molecule-1 to attenuate the inflammatory response (18, 21, 22). The gene discussed is NEO1; the disease is experimental autoimmune encephalomyelitis.