To further evaluate the hypothesis that additional rare and common genetic variation may be necessary for the Dravet syndrome phenotype in some individuals with SCN1A variants, a post hoc exploration with PRS and burden analysis was undertaken, comparing individuals with Dravet syndrome with a GEL SCN1A control cohort composed of 45 GEL probands with unique SCN1A missense variants, but without epilepsy (Supplementary Table 4). This evidence concerns the gene SCN1A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.