We used two media conditions35 and five isogenic lines; the control wild-type, two previously published LIS1+/− lines10, LIS1 overexpression (OE), and a lissencephaly-associated intronic mutation in intron 6 affecting splicing38 (LIS1-int6*/*) in the homozygous form, that slightly reduced LIS1 levels (Fig. 1e, Supplementary Fig. 3a–c). This evidence concerns the gene PAFAH1B1 and Lissencephaly.