In recent years, pathophysiological mechanisms underlying the wasting of skeletal muscle and adipose tissue during cancer cachexia have been investigated intensely, and key processes and therapeutic targets have been identified, including pro-inflammatory mediators (e.g., IL-6, TNF-α, IL-6, IL-1, and IFN-γ) and proteolysis mediators (e.g., myostatin, proteolysis-inducing factor, angiotensin II, and the ubiquitin–proteasome system) secreted from the tumor cell themselves and host cells in response to tumors [8, 10, 11]. Here, MSTN is linked to neoplasm.