Prior work has established that Dravet syndrome (DS) is largely due to heterozygous pathogenic loss-of-function variants in SCN1A leading to haploinsufficiency of the voltage-gated sodium channel α subunit Nav1.1 (Claes et al., 2001). This evidence concerns the gene SCN1A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.