PRDM12 and hereditary sensory and autonomic neuropathy: However, in the original paper, two families with several affected members had expanded PRDM12 polyalanine tracts; family A showed a CIP phenotype with a homozygous 19-alanine expansion (19A); family J had features of MiTES in early childhood and, later, partial CIP with a homozygous 18-alanine expansion (18A).1,7,9–11