Alterations in other proto-oncogenes such as H-RAS, v-SRC and AKT induce increased rates of aerobic glycolysis indirectly through increased expression of HIF-1α and thus its targets [440–442], as well as some angiogenic factors (such as vascular endothelial growth factor (VEGF) and erythropoietin (EPO) [443]), required for survival and tumour growth. Here, AKT1 is linked to neoplasm.