Voltage-gated sodium channels produce action potentials that carry pain sensation into the central nervous system. Here is an article about a family with members who exhibit a congenital inability to experience pain:
In a more recent article, two sodium channel mutations were reported that cause reduced expression of Nav1.7 at the cell surface and disrupt the ion transport function: Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations.
Minor variations in Nav1.7 structure can cause subtle alterations in sodium channel function and pain sensation (1). Pharmacological agents such as ranolazine are being investigated for possible use as inhibitors of pain sensation (2).