Specifically, frequent change targeting in glioblastoma cells, such as mammalian target protein phosphoinositide 3-kinase/protein kinase B/rapamycin (PI3K/AKT/mTOR), p53 and retinoblastoma (RB) pathways, epidermal growth factor receptor genes, and amplification or mutation failure can improve the prognosis. The gene discussed is AKT1; the disease is glioblastoma.