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Nav1.8 is a voltage-gated sodium channel and plays a critical role in the generation and conduction of action potentials and is thus important for electrical signaling by most excitable cells. Therapeutically, the association of pain insensitivity with the loss of function of a certain sodium channel may have implications. Since Nav1.8 is not present in cardiac muscle or neurons in the central nervous system, blockers of Nav1.8 will not have direct action on these cells and thus can have less side effects than current pain medications. By performing more studies, there is a possibility to develop a new generation of drugs that can reduce the pain intensity in animals (3).