This assumption was recently challenged by selectively deleting the TGF‐type‐II receptor in MFS mice (Fbn1C1039G/+) suggesting that increased TGF‐beta in MFS may not be the sole cause of MFS aortopathy.14 Consequently, these results suggest that there may be previously unrecognized mechanisms, by which MFS disease progression is regulated and potential etiologies of MFS need further examination. The gene discussed is TGFB1; the disease is Marfan syndrome.