In most cases, METTL3 exerted oncogenic or tumor suppressive functions through deposition of m6A. In highly lethal colorectal cancers, METTL3 was sufficient to stabilize HK2 and GLUT1 expression in an m6A-IGF2BP2/3 manner to accelerate tumor progression [23]. This evidence concerns the gene SLC2A1 and colorectal cancer.