Previous studies have provided adequate evidence that the KEAP1/nuclear factor erythroid 2-related factor (NRF2) antioxidative signaling pathway is a key negative regulator of ferroptosis in tumor cells through the transcriptional activation of genes involved in ROS and iron metabolism, such as SLC7A11 and NQO1,30, 31, 32 thus supporting our hypothesis of KEAP1’s potential function in promoting CDDP/PEM-induced ferroptosis and the acquisition of chemoresistance. This evidence concerns the gene KEAP1 and neoplasm.