The Drosophila paralytic gene is much less homologous to human sodium channels, with 57% identity to SCN2A and 47.5% identity to SCN1A. However, Sun et al. [80] and Schutte et al. [81] were able to recapitulate temperature-sensitive seizure phenotypes in Drosophila using knock-in mutations homologous to Dravet-causing mutations in human SCN1A. These models were subsequently used to further elucidate neural dysfunction in Dravet syndrome. Here, SCN1A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.