The CPM lesions characterized by AQP4 and AQP1 loss, but preserved GFAP staining of astrocytes in the absence of antibodies, complement activation or AQP4 astrocyte internalization, somewhat resemble the type 6 NMO lesions recently described which show a more pronounced loss of AQP4 and AQP1 than GFAP, and also occur in the absence of immunoglobulin deposition or complement activation [27]. This evidence concerns the gene GFAP and neuromyelitis optica.