BACH1 and familial pancreatic carcinoma: 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).