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]. This evidence concerns the gene AGTR2 and Stroke.