Indeed, a recent finding of almost 100 unique missense SCN1A mutations challenges the previously held notion that haploinsufficient SCN1A mutations alone are responsible for Dravet syndrome because many of these missense mutations likely confer only partial, rather than complete, heterozygous loss of function [22]. Here, SCN1A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.