A study in humans showed that patients with lissencephaly carrying RELN mutations in splicing recognition sites also exhibited cerebellar hypoplasia due to a decrease in full‐length reelin,8 in agreement with the features such as altered neuronal differentiation and migration observed in our in vitro phenotypes.44 Specifically, we showed severe structural defects in homozygous Reln‐del cultures (Fig. 5c and Movie S4), which closely associate with cerebellar hypoplasia,8 indicating a potentially reliable lissencephaly model. The gene discussed is RELN; the disease is Lissencephaly.