Half of NMO cases showed a pronounced loss of Cx43, almost in parallel with the diminution of AQP4 in active lesions, whereas oligodendrocytic Cx47, a major partner of astrocytic Cx43 in heterotypic A/O GJs [38–41], and other myelin proteins including MAG, Cx32, OSP, MBP and MOG were still preserved. This evidence concerns the gene CLDN11 and neuromyelitis optica.