Our finding that mnb overexpression slows replenishment of the readily releasable pool of vesicles, and also modifies basal synaptic transmission, confirms a previous suggestion that DYRK1A overexpression contributes to synaptic dysfunction and cognitive deficits associated with DS, made on the basis of the observed slowing of endocytosis of transmitter vesicles in cultured mouse hippocampal neurons overexpressing human DYRK1A (Kim et al., 2010). This evidence concerns the gene DYRK1A and Dravet syndrome.