It has been reported that VIP can effectively increase the number of Treg subpopulations while decreasing the number of Th17 subpopulations to improve inflammation in asthmatic mice by regulating Th17/Treg balance and VIP can also maintain the immune balance between Th17/Treg cells in the prevention and treatment of experimental autoimmune encephalomyelitis (EAE). The gene discussed is VIP; the disease is experimental autoimmune encephalomyelitis.