Activation of the pathway is frequently detected in LGG and secondary glioblastoma, either as a result of enhanced platelet-derived growth factor (PDGF) signaling (via receptor amplification/mutation or ligand overexpression) or due to inactivation of the regulatory inhibitor PTEN (via PTEN promoter methylation and silencing)38–40. The gene discussed is PTEN; the disease is glioblastoma.