It has been found that the activation of PDGFR-signaling via a PDGF-nitric oxide (NO)-ID4-regulatory circuit (155) in humans accounts for tumorigenesis in 30% of GBM patients, and the overexpression or alterations of PDGF ligands are commonly found in GBM patients, especially in a proneural subtype of GBM, which contributes to the development of GBM and the function of GSCs, such as the self-renewal and tumor-initiating capacity to different extents among PDGFRα and PDGFRβ (155). This evidence concerns the gene PDGFRA and glioblastoma.