Unlike GluA2 global knockout (KO) mice, which suffer from severe motor performance deficits including ataxia (Gerlai et al., 1998, Jia et al., 1996), mice that lack AMPAR subunit GluA1 or GluA3 (GluA1-KO and GluA3-KO) displayed intact basic motor behavior (Figure S1). This evidence concerns the gene GRIA2 and cerebellar ataxia.