GRM1 and cerebellar ataxia: Indirect evidence for a pathogenic role of the antibody comes from the demonstration of mGluR1-specific plasma cell clones within the CNS [33, 35] and from the fact that fading of ataxia after immunotherapy was paralleled by disappearance of the antibody [33]; by contrast, persistence of ataxia was accompanied by persisting serum and CSF anti-mGluR1 in a second patient [33].