SCN1A and Dravet syndrome: The cellular basis for many features of DS including seizures and premature death appears to involve disinhibition, as global deletion of Scn1a suppresses activity of inhibitory but not excitatory neurons in the cortex and hippocampus (Yu et al., 2006; Dutton et al., 2013), and conditional deletion of Scn1a from forebrain inhibitory neurons results in a DS-like phenotype similar to global Scn1a deletion (Cheah et al., 2012).