DYRK1A and Dravet syndrome: Although EGCG was originally administered in the DS setting for its ability to inhibit DYRK1A activity, the field has largely failed to determine whether EGCG treatment – usually administered as part of a supplement either to trisomic mice or to individuals with DS – actually improves the behavioral and cellular deficits via inhibition of Dyrk1a activity, the putative mechanism of its effects.