Muscle wasting is one of the hallmarks of cancer cachexia which involves proteolysis mediated by the ubiquitin-proteasome pathway (UPP) through cytokine activated signaling molecules like NF-kB, the p38MAPK or JAK-STAT3 pathway and the autophagy-lysosome pathway (ALP) [16, 17] Toll-Like receptor 4 (TLR4), a transmembrane receptor expressed on immune cells and skeletal muscles have also been shown to act as central mediator in cachexia pathophysiology, both for cancer-induced muscle protein breakdown and increased release of cytokines [18]. This evidence concerns the gene STAT3 and cancer.