SCN1A and Dravet syndrome: Case #27 carried a splice donor variant (c.2589+3A>T), predicted to alter splicing and result in loss of function, consistent with the observed DS phenotype This variant profile likely explains the predominance of DS in our cohort, as such variants are known to cause severe haploinsufficiency of the SCN1A-encoded Nav1.1 sodium channel, leading to early-onset febrile and afebrile seizures, multiple seizure types, developmental delay, and characteristic EEG abnormalities.