The unchanged action potential amplitude and Nav1.7 protein expression in lupus mice, combined with a significant reduction in action potential thresholds in nociceptive sensory neurons, strongly suggest that the heightened excitability in nociceptive sensory neurons associated with chronic pain induced by SLE is likely due to alterations in voltage-gated mechanisms rather than changes in the protein expression levels of Nav1.7. The gene discussed is SCN9A; the disease is systemic lupus erythematosus.