METTL3 and colonic neoplasm: In the former study, METTL3 was found to promote GLUT1 translation in an m6A-dependent manner by integrative m6A sequencing, RNA sequencing, and ribosome profiling analyses, resulting in increased glucose uptake and lactate production which subsequently activated mTORC1 signaling; consequently, depletion of METTL3 impaired the self-renewal capacity of colon cancer-initiating cells (Chen et al., 2021).