STK11 and cancer: One of the explanations for this failure is that blocking hyperactive RAS/RAF/MEK/ERK signaling by MAPK inhibitors in RAS/RAF-mutated cancer cells elevates autophagic flux through relieving LKB1/AMPK/ULK1 (LKB1, liver kinase B1, ULK1, Unc-51-like autophagy-activating kinase) axis and inhibiting glycolysis and mitochondrial functions, which leads to drug tolerance and/or acquired resistance [265].