Instead, we found that NRF2, another potent regulator of ferroptosis 26, 27, mediates the ferroptosis downstream of CPEB1 in pancreatic cancer based on the following findings: First, we detected the protein abundance of NRF2 (a key transcription factor in response to oxidative stress) and BACH1 (a transcriptional repressor antagonistic to NRF2 28) in the CPEB1-ko and -normal cells by immunoblotting, and found that CPEB1 loss remarkably upregulated NRF2 without affecting BACH1 (Figure 2A), whereas overexpression of CPEB1 complementarily downregulated NRF2 (Figure 2B). This evidence concerns the gene BACH1 and pancreatic neoplasm.