Sottoriva et al. describe GBM evolution at an individual patient level with the founding clone displaying amplification of EGFR, cyclin-dependent kinase 6 (CDK6), and mesenchymal-epithelial transition factor (MET), and a loss of cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) and phosphatase and tensin homolog (PTEN), subsequently giving rise to sub-clone populations manifesting in later mutations, such as loss of NF-1 and TP53 [9]. This evidence concerns the gene EGFR and glioblastoma.