As representative examples, differentiation of CD133+ GBM cells with bone morphogenetic protein 4 (BMP4) or using an all-trans retinoic acid (ATRA)-based treatment led to inhibition of the tumorigenic potential of these cells and resulted in retardation of GBM growth in mice, as well as in sensitizing cells to radiation and BCNU chemotherapy in the case of ATRA [7,8]. The gene discussed is PROM1; the disease is glioblastoma.