Thus, the Lin28/let-7 axis sits firmly at the interface of metabolic reprogramming and malignant growth, which is consistent with recent works, for example showing: that the Lin28/let-7 axis facilitates aerobic glycolysis while inhibiting mitochondrial oxidative phosphorylation in hepatocellular carcinoma30; that Lin28B enhances glycolysis and lactate secretion to promote cancer stemness31; and that Lin28 promotes de novo fatty acid synthesis in liver cancer32. Here, LIN28A is linked to cancer.