Primary GBMs are often characterized by mutations in the phosphatase and tensin homolog deleted on chromosome ten (PTEN) range and EGFR amplification, while, in secondary glioblastoma, we are more often dealing with TP53 mutations [8,176,237,238,239,241,242,243,244,245,246,247,248]. Here, EGFR is linked to glioblastoma.