AMPK activation has been suggested to inhibit tumour cell growth, and this may likely reflect in silo activation of the AMPK signalling pathway, which then leads to p53-dependent cell growth arrest.22–24 On the contrary, AMPK activation in the contexts of cellular survival, in this case represented by hypoxia, contributes to p53-independent TAp73 activation and consequent angiogenic target gene transactivation. This evidence concerns the gene PRKAA1 and neoplasm.