By utilizing a mouse model of Marfan syndrome (MFS) defined by a mutation in the Fibrillin-1 (FBN1) gene, researchers have discovered a connection between mitral valve pathology and the enhanced activity of transforming growth factor-β (TGF-β) (13), which plays a significant fibrotic role in MVP development. This evidence concerns the gene FBN1 and familial mitral valve prolapse.