Almost all previously reported individuals with MiTES were also PRDM12 18A homozygotes (Table S2); one sibling pair was suspected of being hemizygous for the 18A repeat,2 and one child was a compound heterozygote for 17A/18A repeats.2 A further child was reported by Noguera-Morel et al. as heterozygous for 16A/18A repeats with a high pain threshold but no other features of CIP.4 The gene discussed is PRDM12; the disease is hereditary sensory and autonomic neuropathy.