In particular, studies in mouse models and in cancer patients have shown that interleukin-6 and -1 (IL-6/IL-1) not only sustain tumor growth, survival and progression (Coussens and Werb, 2002), but also perturb host metabolic homeostasis, leading to cachexia (Baltgalvis et al., 2008; Graziano et al., 2005; Kuroda et al., 2007; Mantovani et al., 2010; Uehara et al., 1989). This evidence concerns the gene IL6 and neoplasm.