The data suggest that treatment of sarcopenia with agents that block the relevant cytokines that activate TAK-1 would not only block the established pro-atrophy effects of NFκB, but would also provide an upstream inhibition of Activin A release, effectively shutting down two pathways that negatively perturb skeletal muscle in sarcopenia and cachexia. The gene discussed is NFKB1; the disease is Cachexia.