Conversely, inhibiting the activity of BCAT2 triggers ferroptosis in cancer cells.[49] Microsomal glutathione S-transferase 1 (MGST1), a selenium-independent glutathione peroxidase, plays a crucial role in safeguarding the endoplasmic reticulum and the outer membrane of mitochondria from lipid peroxidation, thereby protecting cells from ferroptosis.[50] The deletion of the MGST1 gene facilitates ferroptosis in pancreatic cancer cells, and the reexpression of MGST1 restores the resistance of NFE2L2 knockdown cells to ferroptosis. This evidence concerns the gene BCAT2 and pancreatic neoplasm.