GBM was the first tumor characterized by TCGA, whose molecular studies identified three important genetic events in human GBM: 1) dysregulation of growth signaling via amplification and mutational activation of receptor tyrosine kinase (RTK) genes, 2) activation of the phosphatidylinositol‐3‐OH‐kinase (PI(3)K) pathway, and 3) inactivation of the p53 and retinoblastoma tumor suppressor pathways.[10]. The gene discussed is TP53; the disease is neoplasm.