Mutations within the tumour suppressor PTEN, a negative regulator of Akt activation, can result in constitutively active Akt and inhibit FOXO3a, so promoting HIF1 expression, antioxidant gene expression and an increase membrane translocation of glucose transporters and rate-limiting enzymes such as phosphofructokinase-1 [15] (Figure 1). The gene discussed is AKT1; the disease is neoplasm.