Furthermore, this may serve as a potential therapeutic approach to restore p53 in p53-deficient cancers including those in which MDM2 is overexpressed and those with nonsense/frameshift mutations at the C-terminal end of TP53. We tested our hypothesis using MDM2-overexpressing non–small cell lung cancer (NSCLC) and glioblastoma multiforme (GBM) cells bearing WT p53 and p53 mutant NSCLC and breast cancer and urinary bladder cancer cells as models. The gene discussed is TP53; the disease is lung cancer.