DS is one of the best described and genetically most homogeneous DEE syndromes.27 More than 80% of DS cases are attributable to variants in SCN1A3 (OMIM ID: 607208) and about 700 pathogenic CDS variants have been reported.28 Given the clear link between variants in SCN1A and DS, any un-annotated exonic sequence is of potential clinical interest. This evidence concerns the gene SCN1A and Dravet syndrome.