Studies based on these classifications of FBN1 mutations observed limited genotype-phenotype correlations, with the exception of the association of early onset, severe (previously named “neonatal”) MFS and mutations in exons 24–32 [22], and notably the observation of a higher probability of ascending aortic dilatation, aortic event, and mitral valve prolapse in patients with variants altering a cysteine residue [23]. The gene discussed is FBN1; the disease is mitral valve disorder.