Primary GB is typically driven by early genomic alterations such as epidermal growth factor receptor (EGF-R) amplification, telomerase promoter (TERT) mutations, phosphatase and tensin homolog (PTEN) loss, and chromosomal instability, whereas secondary GB or astrocytoma, IDH-mutant often evolves through a stepwise accumulation of mutations, most characteristically IDH1/2 mutations and ATP-dependent helicase ATRX loss. This evidence concerns the gene EGFR and astrocytoma (excluding glioblastoma).