Phenotypic diversity in DS arises from interactions between SCN1A mutations, polygenic backgrounds (e.g., DEPDC5, ALOXE3), epigenetic dysregulation (activated chromatin remodeling genes), and neuroglial/metabolic system perturbations: polygenic variants disrupt mTOR signaling, GABA receptor function, and arachidonic acid metabolism, while astrocytic calcium dysregulation amplifies network excitability via gliotransmitter signaling. Here, SCN1A is linked to Dravet syndrome.