Gene expression profiles across variousstages of Alzheimer’s disease progression showed that KV3.4overexpression (KCNC4) and KV3.1 dysfunction (KCNC1) alter the ioncurrents in neurons and, consequently, synaptic activity, resulting inneurodegenerative sequelae [11].Voltage-gated K+ channel defects (KV7.1 (KCNQ1),KV11.1 (KCNH2), KCNE1, KCNE2) have been associated with the long Q-Tinterval syndrome [12]. Here, KCNH2 is linked to early-onset autosomal dominant Alzheimer disease.