KRAS and pancreatic neoplasm: Additionally, oncogenic KRAS-induced NRF2 could upregulate the expression of glutaminase-1, glutamate oxaloacetate transaminase 1, and cystine/glutamate antiporter SLC7A11 to enhance glutaminolysis and antioxidant capacity, leading to chemoresistance in KRAS-driven pancreatic cancer [24].