Among the RTKs, EGFR and PDGFRα were the 2 earliest ones identified to have amplifications in gliomas.73 Early study also demonstrated a human GBM-derived PDGFRα mutant transcript with an in-frame deletion of exons 8 and 9 in the extracellular domain (PDGFRα (Δ8,9)) that transformed Rat1 cells into oncogenic cells capable of inducing tumor formation in nude mice.14 Further study with GBM also showed that a PDGFRα with a transmembrane domain mutation V536E stimulated Ba/F3 cell growth and signaling via ERK, which can be strongly inhibited by blocking PDGFR activation.15 This evidence concerns the gene EGFR and glioma.