As metabolic ROS is causally linked to mutant KRAS-induced tumorigenicity and requires homeostatic mechanisms to maintain ROS levels within a threshold favorable for tumor development [14, 27–30, 41], the identification of NOP56 and mTOR converging on a role as ROS scavengers reveals an unanticipated metabolic vulnerability in KRAS-mutant cancers. This evidence concerns the gene KRAS and neoplasm.