Previous findings have shown that knock-out heterozygous mice (Atp1a3+/−) exhibit deficits in spatial learning, hyperactivity, and enhanced locomotor activity in response to amphetamine or intracranial kainate administration (Ikeda et al., 2013), but no lasting symptoms of dystonia (Moseley et al., 2007), and that a knock-in of one of the RDP/AHC mutations, D801Y (Atp1a3+/D801Y; Atp1a3tm1.1Tmklh; MGI 6163502), led to the development of features characteristic of both AHC and RDP (Holm et al., 2016; Isaksen et al., 2017). The gene discussed is ATP1A3; the disease is Dystonia.