In addition to its central role in promoting cell survival and inhibiting apoptosis [11–15], the alteration of intracellular signaling through the PI3K/Akt pathway is deemed crucial to achieve a cancer metabolic phenotype through the Warburg effect [16–20], i.e. the upregulation of glycolysis that allows the branching off of glycolytic intermediates to different anabolic pathways to sustain the higher demand of the transformed cells for metabolic inputs to promote proliferation [21–25]. This evidence concerns the gene AKT1 and cancer.