Instead, the receptor tyrosine kinase that was most often altered in the de novo RRD glioblastomas was PDGFRA (4/9, 44%), with three tumors harboring known activating missense mutations (p.D842Y, p.D561D, p.E229K) in the absence of PDGFRA gene amplification and a fourth tumor with low-level amplification of a mutant PDGFRA allele (p.D842V). Here, PDGFRA is linked to neoplasm.