We demonstrate that both pain and markers of ER stress are reversed by a chemical chaperone.

We aimed at identifying mutants with preserved transport activity but with improper plasma membrane localization for rescue by the chemical chaperone 4-phenylbutyrate (4-PBA).

Chemical chaperone therapy and gene therapy hold promise for the future.

Chemical inducers of ER stress invariably lead to pain behavior that is reversed by a chemical chaperone and an inhibitor of sEH.