In summary, the results of this pilot GWAS provide novel evidence for increased arrhythmic SCA risk in the setting of CAD due to genetic variation in six genes without prior evidence of cardiovascular effect (ACYP2, ZNF385B, GRIA1, AP1G2, DEGS2, KCTD1) and in a number of genes with strong prior evidence of arrhythmic and/or cardiovascular effects (ESR1, CACNA1C, NOS3, NOS1AP, CSMD2, AGTR1, KCNQ1, KCNE1). Here, AP1G2 is linked to autosomal dominant cerebellar ataxia.