Analysis of genome-wide copy number aberrations (CNAs) revealed heterogeneity in putative GBM drivers including gain/amplification of PDGFRA, MDM4, and AKT3, and deletion of PTEN. Reconstruction of tumour fragment phylogenies to infer GBM evolution based on common, shared, and unique genetic events, identified CNAs in EGFR and CDKN2A/B/p14ARF as early trunk events followed by amplification of PDGFRA and deletion of PTEN as subsequent branching events [4]. The gene discussed is PDGFRA; the disease is neoplasm.