Although there is only some evidence to demonstrate that IL-6 can lead directly to lipid mobilization or skeletal muscle protein turnover, there is general acceptance from both mouse [78] and human studies [79] that IL-6 is produced from activated macrophages and acts as a mediator of cancer cachexia by stimulating the liver to induce an acute phase response, with the overproduction of proteins (such as C-reactive protein) [70]. The gene discussed is IL6; the disease is cancer.