GAD2 and stiff-person syndrome: While in T1 D GAD65-Ab are mostly considered as indicators of islet autoimmunity, in SPS a pathogenic role of GAD65-Ab has been postulated based on the finding that they inhibit the enzyme activity of GAD65 in vitro [5,6], and their potential interference with GAD65-mediated transport of GABA-containing vesicles to the presynapse [7,8], both of which may lead to the reduced GABA levels detected in cerebrospinal fluid and brain of SPS patients [9].