The difference in the outcome of our model and the other two is either because of the SHH-activating mutations (SmoM2 vs SmoA1 expression or Ptch1 loss) or more likely because when all GCPs lack a copy of Pten and have activated SHH-signaling that the microenvironemnt provides an advantage for Pten heterozygous cells to form a differentiated tumor. This evidence concerns the gene PTCH1 and neoplasm.