SHH and holoprosencephaly: These findings indicate that growth-based morphogenetic mechanisms such as oriented cell division and/or differential growth are not core mechanisms for OV elongation and that, beyond regulation of cellular states in terms of differentiation and patterning, the relationship between SHH signaling and polarized cell dynamics that induces tissue-level anisotropic deformation is key to elucidating critical pathogenic mechanisms of cyclopia in SHH-deficient embryos.