Paradoxically, it has been recently reported that PKM1 accelerates the glucose catabolism including both glycolysis and TCA cycle, and more importantly, enhances the malignant potential of N-Myc-driven neuroendocrine tumors such as SCLC via efficient mitophagy, the selective autophagy-dependent degradation of old and dysfunctional mitochondria generating cytotoxic ROS [142]. This evidence concerns the gene MYCN and neuroendocrine neoplasm.