Similar blockade of myostatin and activins or genetic myostatin deficiency also prevented muscle wasting and improved survival in LLC and ApcMin/+ (multiple intestinal neoplasia of the murine Apc locus) models of cancer cachexia [105], as well as in inhibin-deficient mice [10,110], although in those cases, tumor growth was also partially inhibited, therefore likely playing a role in improving survival (see also Section 3.6). Here, MSTN is linked to neoplasm.