In previous work, we showed that Scn1b-null mice have reduced expression of Scn1a mRNA and Nav1.1 protein in somatosensory cortex and hippocampus, despite their Scn1a+/+ genotype, suggesting an additive mechanism for the severity of the Scn1b-null model via disrupted regulation of another gene critical in DS (9, 28). The gene discussed is SCN1A; the disease is Dravet syndrome.