GDF2 and hereditary hemorrhagic telangiectasia: The observation that patients treated with TRC105 develop mucosal telangectasias, the hallmark of HHT, in a dose-dependent manner [48] is significant: it demonstrates that ENG-mediated BMP9 inhibition is a likely etiological mechanism underlying HHT; and it provides an easily monitored on-target pharmacodynamic marker of biological response in treated patients.