The main molecular and genetic features of primary GBM are represented by: amplification of epidermal growth factor receptor (EGFR), deletion or mutation of homozygous cycline dependent kinase (CDK) inhibitor p16INK4A/(CDKN2A), alterations in phosphatase and tensin homolog (PTEN) on chromosome 10, and deletion in the INK4 α [7]. This evidence concerns the gene CDKN2A and glioblastoma.