Adults with high anti-GAD antibody concentrations have well-defined clinical phenotypes including stiff-person syndrome, cerebellar ataxia, epilepsy, and limbic encephalitis in adults (Baizabal-Carvallo, 2019; Munoz-Lopetegi et al., 2020), while those with low antibody concentrations present with diverse neurologic syndromes (Saiz et al., 2008; Nanri et al., 2013). Here, GAD1 is linked to cerebellar ataxia.