To further identify the mechanisms by which FOLR1 knockdown impairs apical constriction and induces NTDs, we assessed histologically NTD-affected embryos and find that in addition to the open neural tube (Fig. 2c; Supplementary Fig. 3b), defects range from absence of distinguishable lumen (Supplementary Fig. 3c), lack of neural plate folding (Supplementary Fig. 3d), rounded and loosely attached neural cells (Supplementary Fig. 3d, e), as well as disruptions to neural tissue integrity (Supplementary Fig. 3e), all suggestive of deficient cell-cell adhesion. The gene discussed is FOLR1; the disease is neural tube defect.