In addition, genetic knockdown of PDGFRα in p-CSC2 caused slowdown of cell growth rate and exogenous PDGFAA stimulation of starved GBM CSC promoted p-Erk1/2 and p-Akt1 activation in p-CSC, confirming the concept that PDGFRα activation provided survival signals in p-CSC vs. c-CSC. Here, AKT1 is linked to glioblastoma.