Here, we have used SB mutagenesis to define a novel neuronal transcription factornetwork involved in medulloblastoma formation within the Ptch+/- model, and provide evidence that disruption of this networkupregulates Igf2, critical for proliferation of GNPs and tumour formation.Moreover, we have identified rational therapeutic targets for SHH subgroup tumours,alongside prognostic biomarkers for the identification of poor-risk SHH patients,supporting the further development of these findings as a basis for improved andindividualised therapy. This evidence concerns the gene IGF2 and neoplasm.