Mice with heterozygous deletion of Scn1a reproduce many DS phenotypes, including epilepsy with early onset (Yu et al., 2006; Ogiwara et al., 2007), susceptibility to febrile seizures (Oakley et al., 2009), sleep and circadian abnormalities (Han et al., 2012a; Papale et al., 2013), and premature death (Kalume et al., 2013). The gene discussed is SCN1A; the disease is epilepsy.