By employing bidirectional chemogenetic manipulation, we identified VAL CaMKIIα‐positive neurons as pivotal regulators of stress‐induced pain hypersensitivity: Selective inhibition of these neurons in CRS mice reversed multidimensional hyperalgesia, whereas their activation in naive animals recapitulated key pathological pain states, confirming both necessity and sufficiency of this neuronal population in mediating chronic stress‐associated nociceptive sensitization. The gene discussed is LINC01546; the disease is congenital rubella syndrome.