Conceptually, while promoting AT2 receptor mediated neuronal outgrowth could be beneficial after certain pathologies (e.g. stroke), aberrant or collateral neuronal regeneration with hypersensitivity may underpin some painful conditions in the periphery mediated via AT2R [22], in accord with our clinical efficacy data with EMA401 in postherpetic neuralgia patients, and human DRG nociceptor models in vitro [3, 4]. The gene discussed is AGTR2; the disease is postherpetic neuralgia.