Our findings support the hypothesis that p53 plays an important role in the feedback regulation of chemosensitivity in NSCLC, and that p53 mutation attenuates CDDP-induced ROS elevation, suppression of EGFR/PI3K/AKT signaling and apoptosis in chemoresistant NSCLC cells. Here, AKT1 is linked to non-small cell lung carcinoma.