We hypothesized that the simultaneous use of EGFR-targeted therapy with the tumour metabolism inhibitor PENAO would intrinsically double-block tumour metabolism and energy supply by targeting glycolysis via EGFR-PI3K/AKT-HKII signalling [54] whilst perturbing mitochondrial oxidative phosphorylation via PENAO-ANT, as well as induce the mitochondria-mediated apoptosis in cancer cells [38, 45]. The gene discussed is AKT1; the disease is neoplasm.