Furthermore, NR enhanced VSMC-contractile phenotypes, as indicated by increased F-actin polymerization in FBN1-silenced cells modeling Marfan syndrome, as well as in ACTA2R179H and TGFBR2G357W VSMCs (Figure 3A,B), while also reducing the expression and activity of matrix metalloproteinases and other secretory markers (Figure 3C,D). The gene discussed is FBN1; the disease is Marfan syndrome.