These findings therefore imply that (i) CD133+ GSC cells may be clinically dormant/quiescent prior to undergoing proliferative cell division (PCD) to produce CD133- glioblastoma effector progeny, (ii) the dormant like phenotype may allow CD133+ GSC to escape from cell cycle-targeted radio-chemotherapy and regenerate new tumors, and (iii) genes guarding the pools and tumorigenic potential of GSC may not be in the subgroup of genes directly controlling cell proliferation, but in the subgroup regulating cellular quiescence, development, differentiation, and survival. Here, PROM1 is linked to glioblastoma.