We speculate that Purkinje neuron mitochondrial dysfunction and subsequent Ca2+ overload, coupled with a diminished expression of GABA-synthesising GAD enzyme in their axonal terminals, would have led to a perturbation in GABAergic neurotransmission and reduced inhibition of the DCN, which would explain an increase in c-Fos-positive DCN neurons and ataxia phenotype. The gene discussed is FOS; the disease is Ataxia.