SLC7A11 inactivation, genetically or pharmacologically, was shown to potently induce lipid peroxidation and ferroptotic cell death in pancreatic cancer cells (Daher et al., 2019; Badgley et al., 2020); further studies using genetically engineered mouse models (GEMMs) demonstrated that deletion of Slc7a11 significantly suppresses oncogenic Kras-driven PDAC development with ferroptosis induction in Slc7a11-deficient pancreatic tumors with oncogenic Kras activation (Badgley et al., 2020), suggesting that SLC7A11-mediated ferroptosis suppression likely contributes to KRAS-driven PDAC development. This evidence concerns the gene KRAS and pancreatic neoplasm.