Additionally, larvae with a homozygous loss-of-function mutation in the paralogue scn1laa gene (scn1laasa1674) exhibit spontaneous seizures (Griffin et al., 2017), as does a second N-ethyl-N-nitrosourea (ENU)-generated scn1lab mutant (scn1labsa16474) (Eimon et al., 2018) supporting the etiology underlying the spontaneous seizures observed in DS patients results from haploinsufficiency of the Nav1.1 sodium ion channel. The gene discussed is SCN1A; the disease is Dravet syndrome.