Radial glia scaffold disorganization due to knock-out of the transcription factor Nf1b leads to a lack of a specific hippocampal GFAP-positive glial population, lack of hippocampal fissure and DG without affecting cell proliferation, CRC differentiation or Wnt signalling [60]; this suggests that the loss and disorganization of GFAP-positive cells, seen in our mutants specifically in the developing hippocampus (figure 3), might constitute a cellular mechanism contributing to the defective DG development in early Sox2 mutants. This evidence concerns the gene NFIB and colorectal carcinoma.