KRAS and neoplasm: In NSCLC, K-Ras mutations can induce nuclear factor-erythroid factor 2-related factor 2 (NRF2) gene transcription through TPE response elements, upregulating the NRF2 pathway, leading to excessive activation of an antioxidative stress pathway, reducing cisplatin-induced reactive oxygen species (ROS) generation in tumor cells, reducing the mortality of tumor cells, and therefore causing tumor cells to become resistant to cisplatin [66].