KCNQ2 and epilepsy: Epilepsy-causing mutations were also densely distributed in the pore-forming domain of KCNQ2, and these mutations always lead to a LOF by impairing transmembrane potassium conduction [8, 21, 39]; a recent work by Wu et al. [40] revealed a similar distribution pattern in deafness-related KCNQ4 mutations, characterizing the function of KCNQ4 missense mutations on a large scale.