An integrated analysis of the genetic alterations, performed by the TCGA research network, confirmed that the most commonly disrupted signaling cascades in GBM include changes in pathways related to receptor tyrosine kinase (RTK) signaling through the RAS/MAPK (mitogen-activated protein kinase) and PI3K/AKT/mTOR, along with the cell cycle-regulating retinoblastoma (RB) tumor suppressor and p53 pathways. The gene discussed is TP53; the disease is glioblastoma.