Extensive loss of AQP4, along with loss of various connexins (Cx43, Cx32, and Cx47), important for astrocyte-oligodendrocyte interactions, in astrocytes without the characteristic of NMO perivascular deposition of immunoglobulin or activated complement has been described suggesting an underlying astrocytopathy as a contributor of Balo disease pathology (72–74). This evidence concerns the gene GJA1 and neuromyelitis optica.