Established cachexia features a shift toward protein catabolism: amino acids are mobilized for hepatic gluconeogenesis, while insulin resistance promotes proteolysis and lipolysis via inhibition of the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB/AKT) pathway and activation of proteasomal degradation [11,12,13]. This evidence concerns the gene AKT1 and Cachexia.