Given that the genetic ablation or knockdown of Ataxin-2 via the suppression of its physiological roles is able to mitigate and postpone the neurodegenerative process in several disorders (spinocerebellar ataxia type 1, known as SCA1, fronto-temporal lobar degeneration/dementia known as FTLD, amyotrophic lateral sclerosis known as ALS, tauopathies) [55,93,94], it is critical to ask which of the above factors are also modulated in the Atxn2-KO mouse cerebellum. This evidence concerns the gene ATXN2 and spinocerebellar ataxia type 1.