Taken together, our simulations, including Hodgkin–Huxley–like models of all nociceptive sodium channels, suggest a contribution of Nav1.9 to the fast upstroke of the AP and its shoulder formation and proved useful in modelling excitability changes associated with Nav1.7-linked chronic pain syndromes such as erythromelalgia. The gene discussed is SCN9A; the disease is erythromelalgia.