Our results are consistent with the notion that compensatory mechanisms within cerebellar-connected networks might explain the observed decoupling of the primary pathology of SCA1 (cerebellar atrophy) (Klockgether et al., 1998; Schulz et al., 2010; Jacobi et al., 2012) and progression of ataxia. The gene discussed is ATXN1; the disease is Ataxia.