Ultimately, the diversity in genomic and epigenomic drivers among GBM patients, along with the additional variability associated with dynamic ITH, converge on the deregulation of key oncogenic signaling involving receptor tyrosine kinases (RTK), phosphoinositide 3-kinases (PI3K)- protein kinase B (AKT)- mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways. The gene discussed is AKT1; the disease is glioblastoma.