To verify this theory, we conducted a series of in vitro and in vivo experiments to prove that FGL1 facilitates glycolysis and epithelial-mesenchymal transition (EMT) through the phosphatidylinositol 3-kinase (PI3K)/AKT/hypoxia-inducible factor-1α (HIF-1α) pathway, thereby enhancing tumor metastasis. Here, HIF1A is linked to neoplasm.