Considering that DG functions as a “gate” controlling information flow from the entorhinal cortex into the rest of the hippocampus, and hyperexcitability of dentate GCs has long been known as one of epileptogenic mechanisms underlying temporal lobe epilepsy [54, 55], hyperexcitability of GCs caused by downregulation of Kv4.1 may contribute to network abnormalities associated with increased seizure as well as cognitive impairment associated in AD. Here, KCND1 is linked to temporal lobe epilepsy.