Studies in animal models of cancer cachexia revealed that the p38β MAPK-C/EBPβ signaling pathway plays a central role in the activation of muscle catabolism in animal models of cancer cachexia4, 5, whereas the Akt-FoxO1/3 signaling pathway that regulates proteolysis in response to fasting, disuse and denervation is non-essential due to the activation of Akt4, 6. This evidence concerns the gene AKT1 and cancer.