KRAS and neoplasm: KRAS has been shown to drive a metabolic cascade via glutamine-derived aspartate conversion through aspartate transaminase (GOT1), leading to an increased NADPH/NADP+ ratio that helps maintain redox balance in favor of tumor survival.22 Furthermore, oncogenic KRAS can activate the NRF2 antioxidant system, further supporting redox homeostasis.23 In addition, autophagy, a lysosome-mediated recycling process, is upregulated in KRAS-mutant PDAC, and the suppression of KRAS further elevates the already high basal autophagy levels.24,25