Based on these studies, we speculate that the heightened interaction between Mint2 and HCN channels can increase seizure susceptibility because Mint1-knockout mice exhibit enhanced release probability of aminobutyric acid which is protective against epilepsy, amyloid precursor protein-binding-deficient Mint2 variant shows a considerable reduction of the amyloid-β levels which might correlate with the reduction of the epilepsy burden in AD cases, and the fact that the enhancement of the Ih current via lamotrigine can reduce neuronal firing and dendritic excitability. The gene discussed is APP; the disease is Alzheimer disease.