This review intends to provide a comprehensive analysis of the molecular and cellular mechanisms by which dysregulation in the expression, localization, and function of specific NaV channel subtypes (mainly NaV1.7 and NaV1.8) and their auxiliary subunits contributes to aberrant neuronal activation, the generation of ectopic discharges, and sensitization in neuropathic pain. The gene discussed is SCN10A; the disease is neuropathic pain.