The enhanced glycolytic rate can be sustained through the overexpression of glucose transporters [36] and several key glycolytic enzymes [37] mediated by specific activated oncogenes (e.g. PI3K and MYC) and transcription factors (e.g. HIF1), contributing to the acquisition of the Warburg effect and maintaining tumor cell growth and survival [21, 28, 33]. This evidence concerns the gene HIF1A and neoplasm.