Furthermore, VK2 can upregulate glycolysis in bladder cancer cells, mediated by phosphatidylinositide-3-kinase and AKT (PI3K/AKT) and hypoxia-inducible factor-1α (HIF-1α), induce metabolic stress, along with increased phosphorylation of AMPK and reduced phosphorylation of mammalian target of rapamycin complex 1 (mTORC1). This evidence concerns the gene HIF1A and urinary bladder cancer.