Systemic administration of myostatin induces cachexia in mice33, whereas inhibition of myostatin using modified RNA oligonucleotides, systemic administration of the activin receptor extracellular domain/Fc fusion protein (ACVR2B-Fc), and soluble ActRIIB receptor preserve skeletal muscle mass in experimental cancer cachexia34–37. The gene discussed is MSTN; the disease is Cachexia.