In glioblastoma, the Ras pathway has been demonstrated to act as an important signal transduction effector of PDGFR, and abnormal mutation or amplification of PDGFR can trigger MAPK signaling by overactivating Ras, ultimately leading to cytoskeletal remodeling, cell proliferation and proangiogenic growth factor release [9]. Here, PDGFRB is linked to glioblastoma.