DYRK1A and Dravet syndrome: Overexpression of Dyrk1a acts synergistically with GSK3, as a priming kinase, to inhibit NFAT-dependent transcription in cortical neurons stimulated by FGF8 and heart valve elongation during development of the Ts1Cje DS models, through increase in NFAT nuclear export (Arron et al., 2006).