The binding of PDGF to its receptor induces an activation process very similar to that described for EGFR, with receptor dimerization, autophosphorylation, and transduction of signals through the Ras-MAPK, Pi 3Kinase, Src, Stat, and phospholipase C. The overexpression of PDGF and PDGFR is common in secondary glioblastomas [90] apparently due to the decrease of expression of the tumor suppressor TP53. Here, EGFR is linked to glioblastoma.