For these reasons, most studies have used global or inhibitory neuron-specific Scn1a deletions to model DS (Catterall, 2012), with few studies focusing on other high-priority genetic risk factors like Scn1a missense mutations, which represent ~40% of DS-associated mutations (Depienne et al., 2009; Parihar and Ganesh, 2013). This evidence concerns the gene SCN1A and Dravet syndrome.