The human KCNQ2 and KCNQ4 genes encode the pore-forming subunits of Kv7.2 and Kv7.4, respectively. These subunits form heteromeric voltage-gated potassium channels that underlie M-current that regulates repetitive activity in neurons. Mutations in KCNQ2 that reduce M-current are responsible for some forms of benign familial neonatal seizure. KCNQ4 loss-of-function mutations cause hereditary deafness. Kv7.2/Kv7.4 channels are therapeutic targets in seizure and neuropathic pain.