These data add to the recent sequencing data showing that SCN9A is most highly expressed in the rodent C-LTMR population.17 Interestingly many A-LTMRs also show some expression of Nav1.7; however, there is no evidence of impairments either in large fibre-mediated touch modalities or the electrophysiological properties of these afferents in SCN9A-LOF CIP patients.24–26 This is likely due to functional redundancy and the co-expression (unlike in C-LTMRs17) of other TTX-S VGSCs such as Nav 1.1 and 1.6 in these neurons, which can compensate for the loss of Nav1.7.18 Here, SCN9A is linked to hereditary sensory and autonomic neuropathy.