As a whole, the results shown above indicated that in Ptch1+/−/Tis21KO double-mutant mice the PI3K/AKT/mTOR pathway is up-regulated with a model-specific signature in GCPs during cerebellar development and in adult tumor cells, suggesting a pivotal role for the PI3K/AKT/mTOR pathway in the high frequency MB phenotype of the Ptch1+/−/Tis21KO mouse model. This evidence concerns the gene AKT1 and neoplasm.