Furthermore, administration of ACVR2B-Fc as a GDF8/Myostatin inhibitor (ACE-031) in a clinical trial to treat Duchenne muscular dystrophy had to be stopped due to the occurrence of telangiectasias58, typical of deficient BMP9-signaling in the vasculature. This evidence concerns the gene ACVR2B and Duchenne muscular dystrophy.