AMPK signalling may confer suppressive effects on the glycolytic phenotype and cancer progression by forcing mitochondrial activity, but this requires the presence and function of other tumour suppressive mechanisms mediated by p53, PTEN, TSC1/TSC2, and LKB1 which are frequently inactivated in cancer (Jones et al. 2005; Liu et al. 2006). Here, TP53 is linked to neoplasm.