Consistent with its potentially etiological role in DS, Dyrk1A overexpression in mice provokes DS-like neurodevelopmental, visual, motor and cognitive phenotypic alterations (reviewed in Park and Chung, 2013), some of which can be rescued through Dyrk1A normalization (Ortiz-Abalia et al., 2008; Altafaj et al., 2013; Laguna et al., 2013). This evidence concerns the gene DYRK1A and Dravet syndrome.