Notably, we showed decreased expression of Tweak and Fn14 in skeletal muscle of two distinct SMA mouse models during disease progression, which is contrary to previous reports of increased TWEAK/Fn14 activity in experimental models of atrophy in adult muscle [52, 65, 66], suggesting that TWEAK and Fn14 may have distinct roles in skeletal muscle during development and adulthood. The gene discussed is SMN1; the disease is Atrophy.