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Pathogenic expansions of cytosine\u2013adenine\u2013guanine (<jats:styled-content style=\"fixed-case\">CAG<\/jats:styled-content>) encoding polyglutamine tracts account for the largest proportion of autosomal dominant cerebellar ataxias, while <jats:styled-content style=\"fixed-case\">GAA<\/jats:styled-content> expansion in the first introns of <jats:italic>frataxin<\/jats:italic> gene is the commonest cause of autosomal recessive cerebellar ataxias. Currently, there is no available treatment to alter the disease trajectory, with devastating consequences for affected individuals. Inter\u2010 and Intrafamily phenotypic variability suggest the existence of genetic modifiers, which may become targets amendable to treatment. Recent studies have demonstrated the importance of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair pathways in modifying spinocerebellar ataxia with <jats:styled-content style=\"fixed-case\">CAG<\/jats:styled-content> repeat expansions. 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