For instance, a study employing electrophysiological recordings in hippocampal primary neuronal cultures from embryonic (E16–E18) 3xTg-AD mice reported a causative link between the development of hyperexcitability, increased spontaneous synaptic activity, and the reactive oxygen species-dependent appearance of conglomerates of dysfunctional Kv2.1 potassium channels (Frazzini et al., 2016). This evidence concerns the gene KCNA3 and Alzheimer disease.