A possibility for genetic epilepsy, and an as of yet untested strategy, could be to use CRISPR to destroy the splice-site of the recently discovered poison exon (20 N) in SCN1A, in order to permanently upregulate SCN1A expression in Dravet syndrome [18, 19]. Here, SCN1A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.