At the same time, the characterisation of genetic alterations in human gliomas had made significant progress: it was established that glioblastomas were characterised by different combinations of mutations of the tumour suppressors PTEN [62], p53 [61], RB [58], deletions in the INK4a locus [78], thus being unable to make the two INK4a–ARF gene products, p16INK4a and p19ARF, which arrest the cell, or the amplification of CDK4 [78] or epidermal growth factor receptor (EGFR) [79]. The gene discussed is EGFR; the disease is glioblastoma.