Thus, according to the proposed hypothesis, the oxidation of thiol-reactive groups within the mitochondrial OXPHOS complexes by ATO is a critical step resulting in aberrant mitochondrial function and provoking SRPM in KRAS-mutant cancer cells, whereas a high dose VC action leads to a GSH depletion step that eliminates an interference with the ATO’s oxidation action (Figure 6c). Here, KRAS is linked to cancer.