BMI1 has been found to be overexpressed in several cancers and been shown to be crucial for cancer cell survival in medulloblastoma and glioblastoma.10,29–36 Consequently, BMI1 inhibition in human or mouse GBM cells results in impaired CSC self-renewal and absence of tumor formation in grated mice, and this independently of a functional Ink4a locus.29,36 Intriguingly, BMI1 overexpression can confer self-renewal properties and is apparently sufficient to “reprogram” mouse astrocytes into neural stem cells or mouse retinal progenitors into retinal “stem cells”.37,38. This evidence concerns the gene BMI1 and glioblastoma.