MEN1 and Pain: The transcriptional upregulation of the modulatory α5 subunit by menin, the contribution of α5 to high-conductance nAChR channels50, 51, and the enhanced presynaptic clustering of α7-containing nAChRs via C-menin, would all be consistent with the potentiation of nAChR-induced presynaptic facilitation and synaptic hyperexcitability during neuropathic pain.