The extreme microcephaly, contrasted by many well-formed organs outside of the CNS and the co-existence of severe migration arrest and over-migration of cortical neurons in the Lis1-Nde1 double deficient mice, suggests that the neuronal migration defects associated with lissencephaly do not reflect a motility incompetence of the mutant neurons, but rather a non-cell-autonomous guidance error from the RGCs. This evidence concerns the gene PAFAH1B1 and microcephaly.