SCN10A encodes Nav1.8, a tetrodotoxin-resistant voltage-gated sodium channel primarily expressed in peripheral nociceptive neurons 1. This channel plays critical roles in pain signaling and cardiac electrophysiology. In sensory neurons, Nav1.8 mediates neuropathic pain mechanisms and is essential for nociceptor function, with neurons expressing functional SCN10A-dependent sodium currents that respond to nociceptive stimuli 2. The channel also contributes to tissue healing by enabling nociceptor signaling through CGRP release, which modulates immune cell function during wound repair 3. In cardiac tissue, SCN10A variants contribute to conduction abnormalities, and therapeutic overexpression of its short isoform can rescue cardiac sodium current deficits and prevent arrhythmias 4. Mutations in SCN10A are associated with primary erythromelalgia, a rare pain disorder characterized by episodic burning pain in extremities 5. The gene is also implicated in small fiber neuropathy, where SCN10A variants expand the spectrum of genetic causes underlying this condition 6. Recent transcriptomic studies show sex-specific expression differences of SCN10A in spinal motor neurons, suggesting additional regulatory complexity 7. These findings establish SCN10A as a key player in pain processing, cardiac electrophysiology, and tissue repair mechanisms.