It was shown that the genetic deletion of other components of AJs, such as β-catenin and α-catenin, and the cell polarity protein aPKCλ, numb, and numbl destructed AJs in neuroepithelial and radial glial cells of the ventricles and develops hydrocephalus [34], [50], [51], [66], [67]. The gene discussed is NUMB; the disease is Hydrocephalus.