GAD2 and aceruloplasminemia: In support of an epitope-dependent manner of action by GAD65 autoantibodies, it has been demonstrated in vitro that GAD65 autoantibodies in cerebellar ataxia interfere with GABA release, either by inhibiting the packaging of GABA into vesicles and/or by impeding with the shuttling of vesicles [207,208,210], whereas GAD65 autoantibodies in SPSD block the synthesis of GABA [201,205,208].