Importantly, these pathogenic actions of IgGs from patients with anti-GAD ataxia were elicited by the binding of GAD65 with anti-GAD65 Ab itself; these actions were abolished after absorption of anti-GAD65 Ab with recombinant GAD65 [33] while anti-GAD65 Ab elicited no actions in slices from GAD65 knockout mice where inhibitory transmission was mediated by a compensatory effect of GAD67 [30]. The gene discussed is GAD1; the disease is Ataxia.