Our data is consistent with recent reports and observations that ET may represent a family of disorders of neurological channelopathies, with mutations identified in a voltage-gated K+ channel α subunit (the focus of this study) in a family with pure ET2, in voltage-gated sodium channel α subunits in a family with epilepsy and ET (SCN4A)37 and a family with familial episodic pain and ET (SCN11A)38. This evidence concerns the gene KCND3 and epilepsy.