The simplest model explaining the observed pattern is that co-amplification of EGFR and PDGFRA is a driver event early in gliomagenesis prior to the tumor’s rapid expansion phase, and that subsequent tumor heterogeneity arises from random segregation of independent EGFR and PDGFRA double minutes in the daughter cells9, 16, 17. This evidence concerns the gene PDGFRA and neoplasm.