The activation of HIF-1 suppresses the expression of MCT1 while increasing that of MCT4; this maintains an economical use of glucose in the tumour [8] since the lactate produced by hypoxic cells is exported along with hydrogen ions from the cell by MCT4, and can be transported into cells in more oxygenated areas by MCT1 [8, 116]. The gene discussed is SLC16A1; the disease is neoplasm.