The fact that the double mutant showed both enhanced under- and over-migration of cortical neurons also supports the notion that a Lis1-Nde1-DGC multi-protein complex regulates neuronal migration non-cell-autonomously in the RGC rather than in migrating neurons, and that the key cell developmental defect underlying the disorganized cortical layering in lissencephaly is a non-cell-autonomous malfunction of the RGC scaffold. The gene discussed is PAFAH1B1; the disease is Lissencephaly.