Bao et al. (2006a) showed that the CD133+ fraction in D456MG, a pediatric GBM, was enriched after radiation, and the CD133+ GSCs survived radiation by more effectively repairing radiation-induced DNA damage compared to CD133- cells. The radioresistance of the GSCs was reversed by inhibiting Chk1 and Chk2 checkpoint kinases. The adhesion molecule L1CAM (CD171) augmented the DNA damage checkpoint activation which increased radioresistance of GSCs by enhancing Chk2 signaling (Cheng et al., 2011). The gene discussed is PROM1; the disease is glioblastoma.