Previous research has suggested that the pathophysiology of MFS can be explained by ongoing abnormalities in TGF‐beta signalling that lead to progressive destabilization of the aortic wall and it has been suggested that fibrillin‐1 interacts with latent TGF‐beta binding proteins (LTBPs) to restrict TGF‐beta activation.8, 9 Hence, the deficiency of fibrillin‐1 in MFS promotes the release and activation of TGF‐beta. The gene discussed is TGFB1; the disease is Marfan syndrome.