We show that in clinically-distinct cases of Dravet syndrome, with a known SCN1A variant (classified as pathogenic or likely pathogenic in 33/34 cases, and published as pathogenic in the remaining case74), there are examples of blended phenotypes, an excess of rare variants in epilepsy-related genes, and polygenic contributions to the overall phenotype, with additional evidence for genomic resilience (significantly elevated PRS for longevity). This evidence concerns the gene SCN1A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.