Hawkins et al. [204] suggested that the lack of a significant response of first-line DS drugs in the mouse model may have been due to a floor effect, as the untreated Scn1a+/− mice had relatively low spontaneous GTCS incidence and frequencies, so the model was underpowered to identify compounds that significantly reduced spontaneous GTCS frequency within the observation window. Here, SCN1A is linked to Dravet syndrome.