Moreover, metabolic reprogramming with enhanced glutamine dependence in KRAS-mutant lung adenocarcinoma was shown to be promoted through cooperation between the KEAP1/NRF2 system and LKB1, also known as Serine/Threonine Kinase 11 (STK11), which is a tumor suppressor and the major upstream activator of AMPK, establishing a link between energy metabolism and tumor suppression [49]. Here, KRAS is linked to neoplasm.