Snuderl et al. analysed receptor tyrosine kinase (RTK) mutations in glioblastoma and found that around 5% of samples had co-amplification of RTKs, including epidermal growth factor receptor (EGFR), MET and platelet-derived growth factor receptor-α. In several samples these amplifications were not evident in all the tumour cells. Instead, the amplification of specific RTKs indentified subclones within the tumour. Further analyses indicated that the subclones have other genetic mutations in common and are, therefore, likely to have arisen from a common precursor. The clinical implications of these findings have not yet been determined.