Likewise, METTL3 can promote the glycolysis of GC cells through HDG-activated GLUT4 and ENO2, thereby promoting tumor progression (29), and can also attenuate oxidative stress and apoptosis in by regulating the Keap1/Nrf2 pathway (30), implying that METTL3 can regulate cellular oxidative phosphorylation in GC cells. This evidence concerns the gene METTL3 and gastric cancer.