PRDM12 and hereditary sensory and autonomic neuropathy: Aggregation and cytoplasmic mislocalization are common in vitro features of polyalanine expansion disorders, although pathogenicity in vivo is attributed to mutant protein degradation.22PRDM12 expansions associated with CIP are likely to present a similar loss-of-function mechanism at the cellular level, where the absence of nucleoplasmic PRDM12 precludes the development of nociceptors in trigeminal and dorsal root ganglia.