Schematic representation of TIIA blocking glucose metabolism in gastric cancer cells. In tumor cells, glucose is consumed to produce ATP, and the glycolytic intermediates are used for biosynthetic pathways. Proto-oncogene, AKT, stimulates glycolysis and the tumor suppression gene, p53, suppresses glucose metabolism via several pathways. After TIIA treatment, intracellular ATP levels and AKT expression decreases, and p53 expression increases. In the second step of glycolysis, glucose-6-phosphate isomerase, acting as an enzyme, was down-regulated by TIIA treatment. We also found that TIIA dysregulates gluconeogenesis by suppressing LDHB and MDH1 expression, and enhancing PCK2 expression. TIIA promotes the activity of these pathways to suppress cancer cell growth.