One could abruptly divide this cascade into two main points: (1) firstly, the binding of NMO-IgG to AQP4 triggers the functional impairment of astrocytes, quickly completed by a complement-mediated cell destruction; (2) the dysfunction of EAAT2 transporters, as a bystander effect, impairs the clearance of free glutamate which progressively accumulates and initiates an excito-toxic mechanism upon oligodendrocytes, ultimately leading to oligodendrocytes apoptosis and demyelination [11, 53]. Here, AQP4 is linked to neuromyelitis optica.