For instance, individuals with expanded ataxin-1, the protein responsible for spinocerebellar ataxia type 1 (SCA1), but carrying histidine (CAT) interruptions were reported to be phenotypically normal [27], [28], suggesting that interruptions could alter the polyQ properties and reduce the toxic effects. The gene discussed is ATXN1; the disease is spinocerebellar ataxia type 1.