In this regard, recent accumulating lines of evidence have revealed that a subpopulation of glioma stem cells (GSCs), also designated as glioma-initiating cells, expressing stem cell-like markers such as CD133, nestin, CD44, Oligo-2, Oct-3/4, Sox-2, Nanog, Musashi and/or Bmi-1 and endowed with high self-renewal and tumourigenic capacities may be responsible for driving glioblastoma multiforme (GBM) development, local invasion, resistance to current therapeutic treatment and disease recurrence [82, 126, 127, 139–141]. This evidence concerns the gene BMI1 and glioblastoma.