Mutations in other genes encoding ion channels, such as KCNQ2 in benign familial neonatal seizures [9] and SCN1A in Dravet syndrome [10], led to the “channelopathy” hypothesis, which postulates that dysfunction or dysregulation of ion channels is a common mechanism underlying epilepsy syndromes. This evidence concerns the gene SCN1A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.