For example, in two unrelated individuals with Dravet syndrome from this cohort, who share the same SCN1A splicing variant, the milder seizure and cognitive phenotype in one may in small part be explained by their lower epilepsy, and higher intelligence, PRS, respectively (Supplementary Table 6), demonstrating how a more (or less) favourable genetic background may contribute to explaining intra-familial and variant-specific phenotypic heterogeneity, and have bearing on our understanding of disease biology in ‘monogenic’ epilepsies. Here, SCN1A is linked to Dravet syndrome.