To further establish genetic deletion at ITPR1 as the cause of SCA15 we analyzed two additional families with an inherited cerebellar ataxia similar to that described in the AUS1 family, ascertained through neurology clinics in London, United Kingdom. DNA extracted from probands from these two families (family H33 and family H27) were also analyzed using Illumina Infinium HumanHap550 genotyping chips. These experiments showed deletion at the SCA15 locus in all affected members assayed, from SUMF1 through ITPR1. These mutations segregated with disease in these two families (Figure S3). A strategy similar to the one outlined above enabled us to sequence over the breakpoint in family H27 but not family H33. In the former, the deletion spans 344,408 bp, removing exons 1–3 of SUMF1 and 1–44 of ITPR1; in the latter, we estimate that the deletion is 310 kb in length and that it removes exons 1–3 of SUMF1 and exons 1–40 of ITPR1. The site of mutation is of interest, particularly the fact that in each of the three families the telomeric end of the deletion is anchored between exons 3 and 4 of SUMF1; sequence searches failed to identify any repeat sequences that might explain this phenomenon. With three cerebellar ataxia families segregating a SUMF1–ITPR1 deletion, and this deletion not observed in a control population, we may reasonably conclude that the association is causal, and that the deletion is indeed the genetic basis of the disease, with SCA15 the diagnosis in the two British families as well as the original Australian family.