These data are consistent with our previous report of reduced INa density and hypoexcitability of parvalbumin-positive fast-spiking interneurons in Scn1b−/− cortex.27 This observation may provide at least a partial explanation for the increased severity of the Scn1b null model via disrupted transcriptional regulation of another VGSC gene implicated in DS, resulting in an effective double-hit mutation. The gene discussed is SCN1B; the disease is Dravet syndrome.