In GERD, MCs act on receptors on sensory neurons by releasing neuropeptides, such as substance P (SP) and vasoactive intestinal polypeptide (VIP), and pro-inflammatory mediators, such as neurotrophic tropomyosin receptor kinase 1 (NTRK1), drive neuronal plasticity and peripheral sensitization, leading to esophageal nociceptive hypersensitivity and inflammatory responses. This evidence concerns the gene VIP and gastroesophageal reflux disease.