Using mouse models that overexpress Dyrk1a under its endogenous regulatory sequences, mimicking the situation in DS, we now demonstrate that trisomy of Dyrk1a is sufficient to lengthen the G1 phase of the cell cycle and to bias the production of RG-derived neurons and IPs during the early phase of corticogenesis, and that the triplication of the Dyrk1a gene is necessary for dampened early neurogenesis in the developing neocortex of Ts65Dn embryos. The gene discussed is DYRK1A; the disease is Dravet syndrome.