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The paper identifies a frameshift mutation in KCNK18 causing TRESK dysfunction, linking it to neuropathic pain through haploinsufficiency and altered channel function.

This study shows TRESK channels regulate non-histaminergic itch by modulating sensory neuron excitability, and enhancing TRESK function reduces acute and chronic itch in mice.

This study shows that deleting the TRESK K+ channel enhances mechanical and cold sensitivity in mice, indicating its role in regulating neuronal excitability for specific sensory functions.