To understand the mechanism with which silenced BMI1 block tumor formation and to identify new downstream targets, we performed global gene expression profiling in paired CD133+ and CD133− cells derived from 3 models (IC-1406GBM, IC-2305GBM and ICb-1227AA) that expressed high levels of BMI1 at 48 hrs post lentiviral transduction. This evidence concerns the gene BMI1 and neoplasm.