As we found that nAChR α5 gene induction and α7-nAChR clustering are dependent on MEN1 expression, these observations suggest that the molecular actions of menin tune nAChR function by regulating subunit composition and synaptic clustering, and may thus represent a novel cholinergic mechanism underlying injury-induced synaptic plasticity and the development of neuropathic pain. Here, CHRNA4 is linked to neuropathic pain.