We believe this discrepancy can be partially explained by the absence of severe neural tube defects in the Emx1-Cre*Vangl2 cKO, or in a double Vangl1−/−;Foxg1Cre;Vangl2f/f compound cKO (Qu et al., 2014), as compared to mice with germline mutation/deletion such as the Vangl2Lp/Lp mutant or the null Vangl2Δ/Δ mutant (Song et al., 2010), which present with craniorachischisis. This evidence concerns the gene VANGL2 and craniorachischisis.