DS, a severe neurodevelopmental disorder dominated by SCN1A dysfunction, exhibits profound mechanistic complexity: SCN1A mutations disrupt Nav1.1 expression in GABAergic interneurons through transcriptional dysregulation, pre-mRNA splicing defects, and voltage-gated sodium channel dysfunction, leading to impaired inhibitory synaptic transmission and brainwide excitatory-inhibitory imbalance. Here, SCN1A is linked to Dravet syndrome.