For example, although in mice, DS was clearly associated with loss of excitability in interneurons, early studies using iPSC‐derived neuronal cells suggested a counterintuitive GoF effect of the A5768G, Q1923R and F1415I missense mutations in SCN1A, recording increased excitability in both excitatory and inhibitory neurons (Jiao et al., 2013; Liu et al., 2013). The gene discussed is SCN1A; the disease is Dravet syndrome.