No, it is Gain-of-Function Mutation in TRPA1.
A point mutation in the S4 transmembrane segment of TRPA1, a key sensor for environmental
irritants, causes Familial Episodic Pain Syndrome. The mutant channel showed a normal pharmacological profile but altered biophysical properties, with a 5-fold increase in inward current on activation at normal resting potentials.
Check out the fine paper and video that explains the discovery:
A Gain-of-Function Mutation in TRPA1 Causes Familial Episodic Pain Syndrome
More about TRPA1:A role for TRPs in ME/CFS/POTS/MCS/pain/endothelial dysfunction...?
TRP blogposts - an overview