Our computational definition of the SCN1A regulatory elements could be used as a foundation when exploring the status of the individual SCN1A regulatory landscape variation in patients with a pathogenic variant in SCN1A or for other epilepsies for which the use of sodium channel blockers has been proven useful, such as KCNQ2-related encephalopathies (21). This evidence concerns the gene KCNQ2 and Encephalopathy.