A cancer-linked protein called BRAF may help drive chronic nerve pain, and existing cancer drugs targeting it reduced pain sensitivity in preclinical models.

Chronic nerve pain can persist long after an injury and often responds poorly to standard pain medications. Researchers at The University of Texas MD Anderson Cancer Center now report evidence that BRAF, a protein best known for its role in cancer, may also help initiate, intensify, and sustain pain signaling after nerve damage.

In preclinical models, drugs that inhibit BRAF signaling reduced pain sensitivity, pointing to a possible new use for treatments already developed for cancer.