In our current study, we made an intriguing discovery that an initial impairment of Kir4.1 channels occurred in spinal cord oligodendrocyte precursor cells (OPCs) rather than in astrocytes in a mouse model of experimental autoimmune encephalomyelitis (EAE), while the levels of Kir4.1 antibodies in both EAE mouse serum and MS patient serum were significantly elevated. This evidence concerns the gene KCNJ10 and experimental autoimmune encephalomyelitis.