In addition, Karvela et al. demonstrated that pharmacological inhibition of autophagy or downregulation of ATG7, induced a decrease in glycolysis, an increase in oxidative phosphorylation and mitochondrial ROS accumulation thus highlighting ATG7 as a potent therapeutic target in CML [59]. Here, ATG7 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.