In vitro studies have demonstrated that the inhibition of S6K1 signaling leads to increased radiosensitivity in lung cancer cell lines.5,6 S6K1 amplification has also been seen to be associated with resistance to EGFR tyrosine kinase inhibitors treatment resistance and lower recurrence-free survival in EGFR-mutant lung adenocarcinoma.7 This relationship between S6K1 and EGFR treatment resistance was similarly seen in a mouse model study demonstrating that S6K1 signaling allowed tumor cells to overcome EGFR inhibition through MDM2 upregulation. This evidence concerns the gene MDM2 and lung adenocarcinoma.