Thus, altered expression of HCN channels or Ih is a phenomenon regularly observed in models of experimental epilepsy [19], [20], [38], [39], [40], [41], [42], [43], and even in human epilepsy [44], and altered interaction of HCN1 with TRIP8b could be a critical mechanism contributing to this phenomen [20]. This evidence concerns the gene MALAT1 and epilepsy.