Our findings build on two previously reported PDAC-specific characteristics, namely, 1st RAS signaling driving glutamine metabolism for ROS homeostasis22,50,51 and 2nd mitochondrial dependency upon genetic loss of the KRAS oncogene,41 and connect them with a more generally described cancer cell state associated with therapy resistance, characterized by a dependence on lipid peroxidation defense pathways.57,58 Moreover, our work reinforces and extends the concept that PDAC progression and homeostasis rely on the active suppression of ferroptosis.52 This evidence concerns the gene KRAS and cancer.