Despite severe neuronal migration arrest beneath the un-splitted preplate [18], we found that disruption of DGC by the Lis1+/− Nde1−/− mutation also induced type-II lissencephaly-like defects with neuronal “overmigration.” Besides densely packed Cajal-Retzius (C-R) cells in the normally cell sparse marginal zone (MZ) [18], neuronal ectopia outside of the glia limitan were frequently observed in the mutant cortex. The gene discussed is NDE1; the disease is Lissencephaly.