Key mutations found in GBM patients, including the amplification of the epidermal growth factor receptor (EGFR), as well as mutations in the genes encoding phosphatase and tensin homolog (PTEN) and tumor protein 53 (TP53), have been linked to the response to treatments and the accumulation of ROS, which play a significant role in gain-of-function (GOF) activities in cancer cells [18,19]. The gene discussed is TP53; the disease is glioblastoma.