Supporting the idea that excessive TGF-β signaling contributes to the manifestations of MFS, a TGF-β neutralizing antibody significantly improved the lung phenotype in a mouse model of MFS (homozygous Fbn1mgΔ) (Neptune et al., 2003; Cannaerts et al., 2015) and reduced the occurrence of aortic aneurysms in the Fbn1C1039G/+ mouse model of MFS (Habashi et al., 2006). This evidence concerns the gene TGFB1 and aortic aneurysm.