Subsequently, secretory HDGF promoted tumor angiogenesis, and nuclear HDGF activated insulin-responsive glucose transporter 4 (GLUT4) and enolase 2 (ENO2) expression, which in turn promoted glycolysis in GC cells and ultimately promoted cell growth and liver metastasis [139].Lin et al. [140] found that downregulation of METTL3 inhibited the proliferation and migration of human GC cells and inactivated the AKT signaling pathway, a finding that was supported by Liu et al. [141].Low protein expression levels of FTO were correlated with reduced overall survival times in GC patients. This evidence concerns the gene AKT1 and gastric cancer.