The previous review focused on the role of MDM2 in inducing resistance to EGFR-tyrosine kinase inhibitors (TKIs) [1], and then the published research suggested that MDM2 overexpression contributes to resistance to first generation EGFR-TKIs, and EGFR mutant lung adenocarcinoma (LUAD) patients with MDM2 amplification experience poor progression-free survival (PFS) following the administration of these inhibitors [18]. This evidence concerns the gene EGFR and lung adenocarcinoma.