In accordance with the clinical findings of small-fiber atrophy in the tongue (227) and increased expression of TRPV1 in the epithelium of the lingual mucosa of BMS patients (228), this suggests that GFRα3/TRPV1 and artemin-responsive fibers are possible contributors to BMS and that ART-OE mice may be a suitable model for future investigations of the mechanisms underlying BMS. The gene discussed is TRPV1; the disease is burning mouth syndrome.