GUCA1B and cerebellar ataxia: We hypothesize that accumulation of these complexes might result in pathology due to the formation of misfolded GCAP2 oligomers, in much a similar way to which synuclein, APP, Tau, Huntingtin or ataxin lead to neuronal cell death in Parkinson's (PD), Alzheimer (AD), Huntington's (HD) or spinocerebellar ataxia (SCA) diseases.