The functional importance of the glutamate transporters in the cerebellum is highlighted by the appearance of mutations in cerebellar-enriched EAAT1 in human episodic ataxia type 6 [4–6], the down-regulation of EAATs in animal models of the human spinocerebellar ataxias SCA1, 5 and 7 [7–10] and the mildly ataxic phenotype of mice lacking EAAT1 [11]. The gene discussed is SLC1A3; the disease is cerebellar ataxia.