We hypothesize that GBM CSC counteracted angiogenic inhibitory signals by activation of progrowth and prosurvival signals, which comprise PDGF-C, PDGF-D, EDNRB/EDN1/PRKCB1, Bcl-2/Bcl-xL and extracellular signal-regulated kinase (Erk1/2) signaling pathways [8, 32–36]. The gene discussed is BCL2; the disease is glioblastoma.