Inhibition of nuclear factor-κB (NF-κB) signaling in muscle [104] or tumour necrosis factor (TNF)-like weak inducer of apoptosis/ fibroblast growth factor-inducible 14 (TWEAK/Fn14) signaling in the tumor [106], blockade of growth differentiation factor 15 (GDF15) [107], treatment with histone deacetylase inhibitors [109], or counteraction of myostatin and activins [10,11,12,13,105,110] have resulted in prevention of muscle wasting and improved survival in different murine models of cancer cachexia. The gene discussed is INHBE; the disease is Cachexia.