In a mouse model of SHH-MB in which a NeuroD2 promoter drives expression of an oncogenic form of SMO (SmoA1) in the GCP-lineage, heterozygous loss of Pten in all cells (null mutation) or conditional knock-out in Nestin-expressing cells, which includes all cerebellar cells17, leads to increased penetrance and earlier onset of tumor formation with no increase in metastasis12. Here, PTEN is linked to neoplasm.