Elevated plasma levels of angiotensin II are associated with increased production of inflammatory cytokines such as IL-6, IL-8, and TGF-β1, which contribute to the inflammatory state and cause the activation of proteolytic pathways and/or disruption of protein synthesis, thus promoting cancer cachexia.293 Recently, researchers defined a subset of neutrophil-like monocytes, termed cachexia-inducible monocytes, which express CD38+ and induce muscle atrophy by producing IL-36G, thereby exacerbating cachexia phenotypes in advanced cancer models.300. This evidence concerns the gene TGFB1 and Cachexia.