Two genetic mutations linked to congenital analgesia could provide new targets for the development of pain drugs, researchers Geoff Woods and Ya-Chun Chen write. The gene SCN11A affects a protein called Nav1.9 that is linked to the maintenance of cellular voltages that allow pain signals to travel, and SCN9A is key to the process that initiates pain signals between neurons. Based on how different forms of congenital analgesia affect patients, drugs based on these pathways could have side effects like excess sweating or reduced sense of smell.

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