Finally, previous studies of transgenic mouse models of DS have led to the proposal that the overexpression of Dyrk1a (and thus an increased dosage of the DYRK1A protein) makes a critical contribution to neurological and behavioral abnormalities by shifting the excitation/inhibition balance toward inhibition, for example (Ruiz-Mejias et al., 2016, Souchet et al., 2014). This evidence concerns the gene DYRK1A and Dravet syndrome.