The key features of primary GBM include amplification of epidermal growth factor receptor (EGFR) activity, deletion or mutation of homozygous cyclin-dependent kinase (CDK) inhibitor p16INK4A (CDKN2A), alterations in phosphatase and tensin homolog (PTEN) on chromosome 10, and deletion of INK4a [2]. The gene discussed is PTEN; the disease is glioblastoma.