The authors showed that patients with Duchenne muscular dystrophy as well as spinal muscular atrophy have reduced levels of both systemic myostatin and activin (also a negative regulator of muscle mass from the TGF-beta superfamily) while typically having increased levels of circulating follistatin as an important inhibitor of myostatin leading to muscle growth [35, 36]. This evidence concerns the gene INHBE and proximal spinal muscular atrophy.