Conversely, blockade of the ActRIIB receptor prevented cachexia in C26 tumor bearing mice, without affecting increased circulating levels of IL-6, TNF-α, and IL-1β (Zhou et al., 2010), implying ActRIIB signaling acts independent, or downstream of inflammation-associated muscle atrophy through autocrine expression of ActRIIB activating ligands like myostatin or Activin-A (Trendelenburg et al., 2012). The gene discussed is TNF; the disease is neoplasm.