Also, Cav-1 loss significantly downregulated glucose uptake, intracellular ATP and lactate accumulation in colon cancer cells, whereas Cav-1 overexpression increased glucose uptake and ATP production by stimulating HMGA1-medaited transcription of the glucose transporter SLC2A3/GLUT3, which was reported to play a significant role in the development of drug resistance [118]. The gene discussed is SLC2A3; the disease is colonic neoplasm.