SCN1A and Dravet syndrome: The positional specificity of SCN1A intronic variants dictates splicing patterns and phenotypic gradients: canonical splice site variants such as c.602 + 1G > A induce complete exon skipping, leading to near-abolition of full-length mRNA and haploinsufficiency-mediated severe DS, whereas deep intronic variants such as c.4853-25 T > A cause partial exon skipping or intron retention, maintaining higher full-length mRNA levels and correlating with milder febrile epilepsy.