Human pathologies associated with KCNQ channels include cardiac arrhythmias, deafness, and epilepsy. We have shown previously that the KCNQ4 K+ channel underlies a form of dominant human hearing loss (1) and have generated mouse models which showed that this pathology is owed to a degeneration of cochlear sensory outer hair cells (OHCs) that depolarize in the absence of KCNQ4 (3). KCNQ4 localizes to the base of OHCs and is also found at calyx synapses of type vestibular hair cells and selected tracts and nuclei of the brainstem (2). In contrast to cochlear hair cells, KCNQ4 is expressed postsynaptically at vestibular hair cell synapses, where it may contribute to remove K+ from the synaptic cleft (4). Mice lacking KCNQ4 show discrete vestibular symptoms which have also been observed in some humans with KCNQ4-related hearing loss. The expression of KCNQ4 in trigeminal ganglia (2) prompted us to examine its expression in dorsal root ganglia (DRGs). Indeed, we found KCNQ4 to be expressed in a subset of large diameter DRG neurons (5). These innervate a subset of rapidly adapting skin mechanoreceptors, where they localize to sensory nerve endings. Both our Kcnq4 mouse models, as well as patients with KCNQ4 mutations, showed altered skin mechanoreception (5). KCNQ4 tunes the response of mechanoreceptors to their optimal frequencies. KCNQ4 has multiple, rather unrelated roles in sensory biology.