in astrocyte cells, and the concentration of GFAP differs between different regions in the CNS, where the highest levels are found in medulla oblongata, cervical spinal cord and hippocampus. It is involved in many important CNS processes, including cell communication and the functioning of the blood brain barrier. GFAP has been shown to play a role in mitosis by adjusting the filament network present in the cell. During mitosis, there is an increase in the amount of phosphorylated GFAP, and a movement of this modified protein to the cleavage furrow. There are different sets of kinases at work; cdc2 kinase acts only at the G2 phase transition, while other GFAP kinases are active at the cleavage furrow alone. This specificity of location allows for precise regulation of GFAP distribution to the daughter cells. Studies have also shown that GFAP knockout mice undergo multiple degenerative processes including abnormal myelination, white matter structure deterioration, and functional/structural impairment of the blood–brain barrier. These data suggest that GFAP is necessary for many critical roles in the CNS. GFAP is proposed to play a role in astrocyte-neuron interactions as well as cell-cell communication. In vitro, using antisense RNA, astrocytes lacking GFAP do not form the extensions usually present with neurons. Studies have also shown that Purkinje cells in GFAP knockout mice do not exhibit normal structure, and these mice demonstrate deficits in conditioning experiments such as the eye-blink task. Biochemical studies of GFAP have shown MgCl2 and/or calcium/calmodulin dependent phosphorylation at various serine or threonine residues by PKC and PKA which are two kinases that are important for the cytoplasmic transduction of signals. These data highlight the importance of GFAP for cell-cell communication. GFAP has also been shown to be important in repair after CNS injury. More specifically for its role in the formation of glial scars in a multitude of locations throughout the CNS including the eye and brain. Autoimmune GFAP astrocytopathy In 2016 a CNS inflammatory disorder associated with anti-GFAP antibodies was described. Patients with autoimmune GFAP astrocytopathy developed meningoencephalomyelitis with inflammation of the meninges, the brain parenchyma, and the spinal cord. About one third of cases were associated with various cancers and many also expressed other CNS autoantibodies. Meningoencephalitis is the predominant clinical presentation of autoimmune GFAP astrocytopathy in published case series. It also can appear associated with encephalomyelitis and parkinsonism. Disease states There are multiple disorders associated with improper GFAP regulation,