Given the importance of Dyrk1a regulation of major neurodevelopmental processes, and the distinct likelihood that the postnatal trajectory of altered brain structural and functional development in DS has its origins in fetal or postnatal Dyrk1a overexpression, it is essential to identify the substrates or secondary targets of Dyrk1a regulation that are implicated in deleterious neurodevelopmental phenotypes. The gene discussed is DYRK1A; the disease is Dravet syndrome.