KCNK2 and migraine disorder: In conclusion, our results provide evidence of the key role of TREK1 and TREK2 channels in migraine induction by regulating TG excitability, whereas their genetic invalidation induces a neuronal hyperexcitability leading to migraine-like phenotype, their activation suppresses NO-donor induced-migraine phenotype as efficiently as current anti-migraine drugs targeting neuropeptide release.